Forward-looking statements This document contains forward-looking statements. All statements other than statements of historical facts contained in this document, including statements regarding possible or assumed future

Wave Life Sciences Corporate

Presentation April 1, 2021 Exhibit 99.1

Forward-looking statements This

document contains forward-looking statements. All statements other than statements of historical facts contained in this document, including statements regarding possible or assumed future results of operations, preclinical and clinical studies,

business strategies, research and development plans, collaborations and partnerships, regulatory activities and timing thereof, competitive position, potential growth opportunities, use of proceeds and the effects of competition are forward-looking

statements. These statements involve known and unknown risks, uncertainties and other important factors that may cause the actual results, performance or achievements of Wave Life Sciences Ltd. (the "Company") to be materially different

from any future results, performance or achievements expressed or implied by the forward-looking statements. In some cases, you can identify forward-looking statements by terms such as "may," "will," "should,"

"expect," "plan," "aim," "anticipate," "could," "intend," "target," "project," "contemplate," "believe," "estimate,"

"predict," "potential" or "continue" or the negative of these terms or other similar expressions. The forward-looking statements in this presentation are only predictions. The Company has based these

forward-looking statements largely on its current expectations and projections about future events and financial trends that it believes may affect the Company's business, financial condition and results of operations. These forward-looking

statements speak only as of the date of this presentation and are subject to a number of risks, uncertainties and assumptions, including those listed under Risk Factors in the Company's Form 10-K and other filings with the SEC, some of which

cannot be predicted or quantified and some of which are beyond the Company's control. The events and circumstances reflected in the Company's forward-looking statements may not be achieved or occur, and actual results could differ

materially from those projected in the forward-looking statements. Moreover, the Company operates in a dynamic industry and economy. New risk factors and uncertainties may emerge from time to time, and it is not possible for management to predict

all risk factors and uncertainties that the Company may face. Except as required by applicable law, the Company does not plan to publicly update or revise any forward-looking statements contained herein, whether as a result of any new information,

future events, changed circumstances or otherwise.

Building a leading genetic medicines

company ALS: Amyotrophic lateral sclerosis; FTD: Frontotemporal dementia 1stereopure oligonucleotides and novel backbone chemistry modifications Innovative platform Stereopure oligonucleotides Novel backbone modifications (PN chemistry)

Allele-selectivity Multiple modalities (silencing, splicing, ADAR editing) Strong IP position1 Foundation of NEUROLOGY programs Huntington's disease ALS / FTD Neuromuscular diseases Ataxias Parkinson's disease Alzheimer's disease

Clinical development expertise Multiple global clinical trials Innovative trial designs Manufacturing Established internal manufacturing capabilities to produce oligonucleotides at scale Wave's discovery and drug development

PRISM has unlocked novel and

proprietary advances in oligonucleotide design Backbone modifications Sugar modifications Drug approvals (FDA)2 1975 2020 2000 Mixtures of 2n molecules1 ~500,000 different molecules per dose fomivirsen pegaptanib Phosphorothioate (PS) mipomersen

nusinersen PN backbone chemistry modifications Stereopure backbone 2'-4'-cEt 2'-O-methyl 2'-F 2'-4'-LNA 1n=number of chiral centers 2'-MOE Phosphorodiamidate Morpholino (PMO) eteplirsen golodirsen givosiran

patisiran inotersen viltolarsen 2oligonucleotide therapies approved by the FDA across the industry

THERAPEUTIC AREA / TARGET DISCOVERY

PRECLINICAL CLINICAL PARTNER ALS and FTD C9orf72 Takeda 50:50 option Huntington's disease mHTT SNP3 SCA3 ATXN3 CNS diseases Multiple Takeda milestones & royalties DMD Exon 53 100% global ADAR editing Multiple AATD (ADAR editing)

SERPINA1 100% global Retinal diseases USH2A and RhoP23H 100% global NEUROLOGY HEPATIC OPTHALMOLOGY WVE-004 WVE-003 Innovative pipeline led by neurology programs During a four-year term, Wave and Takeda may collaborate on up to six preclinical

targets at any one time. ALS: Amyotrophic lateral sclerosis; FTD: Frontotemporal dementia; SCA3: Spinocerebellar ataxia 3; CNS: Central nervous system; DMD: Duchenne muscular dystrophy; AATD: Alpha-1 antitrypsin deficiency Stereopure PN chemistry

Platform evolution reflected in three

upcoming clinical trials to start in 2021 Variant-selective silencing candidate in ALS and FTD WVE-004 C9orf72 WVE-003 SNP3 Allele-selective silencing candidate in HD WVE-N531 Exon 53 Exon skipping candidate in DMD HD: Huntington's diseaseALS:

amyotrophic lateral sclerosisFTD: frontotemporal dementia DMD: Duchenne muscular dystrophy Oligonucleotide innovation and optimization PN backbone chemistry modifications Interactions between sequence, chemistry and stereochemistry In vivo models

Insight into PK / PD relationships Novel model generation Leverage learnings of first generation programs Translational pharmacology Adaptive clinical trial design

WVE-004 Amyotrophic Lateral Sclerosis

(ALS) Frontotemporal Dementia (FTD)

C9orf72 repeat expansions: A critical

genetic driver of ALS and FTD Normal (non-expanded) Allele < 25 GGGGCC repeats Expanded Allele Sources: DeJesus-Hernandez et al, Neuron, 2011. Renton et al, Neuron, 2011. Zhu et al, Nature Neuroscience, May 2020 Typically 100's-1000's

of GGGGCC repeats C9orf72 hexanucleotide repeat expansions (GGGGCC) are one of the most common genetic causes of the sporadic and inherited forms of Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD) The C9orf72 repeat expansions

also lead to accumulation of repeat-containing transcripts, nuclear sequestration of RNA binding proteins and synthesis of toxic dipeptide-repeat (DPR) proteins The C9orf72 repeat expansions lead to reduced expression of wild-type

C9orf72 and to cellular changes that reduce neuronal viability Neuro C9orf72

C9-ALS and C9-FTD: Manifestations of a

clinical spectrum Disease C9 specific US population Mean disease duration Standard of care C9-ALS Fatal neurodegenerative disease Progressive degeneration of motor neurons in brain and spinal cord ~2,000 3.1 years Significant unmet need

despite two approved therapies in US C9-FTD Progressive neuronal atrophy in frontal/temporal cortices Personality and behavioral changes, gradual impairment of language skills ~10,000 6.4 years No approved disease modifying therapies Two

devastating diseases with a shared genetic basis ALS: Amyotrophic lateral sclerosis; FTD: Frontotemporal dementia Sources: Cammack et al, Neurology, October 2019. Moore et al, Lancet Neurology, February 2020 Neuro C9orf72

C9orf72 repeat expansions:

Mechanisms of cellular toxicity C9-ALS and C9-FTD may be caused by multiple factors: Insufficient levels of C9orf72 protein Accumulation of repeat-containing RNA transcripts Accumulation of aberrantly translated DPR proteins Recent evidence suggests

lowering C9orf72 protein exacerbates DPR-dependent toxicity Sources: Gitler et al, Brain Research, September 2016. Zhu et al, Nature Neuroscience, May 2020 Targeted by Wave ASOs Variant-selective targeting could address multiple potential drivers of

toxicity Neuro C9orf72

Normal C9orf72 allele produces three

mRNA transcripts (~80% are V2, ~20% are V1 and V3) Pathological allele with expanded repeat leads to healthy V2 and pathological V1 and V3 transcript by-products C9orf72 targeting strategy spares C9orf72 protein WVE-004 targets only V1 and V3

transcripts, sparing V2 transcripts and healthy C9orf72 protein pre-mRNA variants Pathological mRNA products V1 V2 Mis-spliced V1/V3 Stabilized intron1 V3 Disease-causing factors RNA foci Dipeptide repeat proteins (DPRs) GGGGCC expansion Accessible

target for variant selectivity WVE-004 reduces Repeat-containing transcripts Neuro C9orf72

PN backbone chemistry modifications:

Improved potency among C9orf72-targeting oligonucleotides in vivo Exposure ( g/g) Exposure ( g/g) C9orf72 compounds Spinal cord Cortex PS/PO backbone PS/PO/PN backbone %C9orf72 V3 transcript remaining Mice received 2 x 50 ug ICV doses

on days 0 & 7; mRNA from spinal cord and cortex quantified by PCR (Taqman assay) 8 weeks later. Oligonucleotide concentrations quantified by hybridization ELISA. Graphs show robust best fit lines with 95% confidence intervals (shading) for

PK-PD analysis. Spinal Cord Neuro C9orf72

WVE-004: Potent and selective

knockdown of repeat-containing transcripts in vitro V3 Dose ( M) All V WVE-004 NTC Dose ( M) In vitro activity in C9 patient-derived neurons WVE-004 NTC Dose ( M) IC50:201.7nM In vitro selectivity in C9 patient-derived neurons C9

patient-derived motor neurons were treated with C9orf72 candidate and NTC under gymnotic conditions up to 10uM. Taqman qPCR assays were used to evaluating V3 and all V transcripts. NTC- non-targeting control. Relative fold change C9orf72 V3/HPRT1

1.5 1.0 0.5 0.0 0.001 0.01 0.1 1 10 Relative fold change C9orf72 V3/HPRT1 0.016 0.08 0.4 2 10 0.016 0.08 0.4 2 10 0.016 0.08 0.4 2 10 0.016 0.08 0.4 2 10 1.5 1.0 0.5 0.0 1.5 1.0 0.5 0.0 Relative fold change C9orf72/HPRT1 Neuro C9orf72

WVE-004 demonstrates durable

reduction of DPRs in vivo after 6 months in spinal cord and cortex Spinal cord Cortex Full results presented at the 31st International Symposium on ALS/ MND (December 2020) Top: 2 x 50 ug (day 0, day 7) dosed ICV; DPRs measured by Poly-GP MSD assay.

*: p 0.05 **: P 0.01, ***: P 0.001. ICV: intracerebroventricular; DPR: Dipeptide repeat protein; Bottom: C9 BAC transgenic mice administered PBS or 50 ug WVE-004, ICV, (day 0, day 7). ns: not significant; PBS:

phosphate-buffered saline * *** ** 4 12 18 12 18 24 4 24 WVE-004 PBS week 1.5 0.5 0.0 1.0 Relative Poly-GP levels (normalized to PBS) p 0.0001 4 12 18 12 18 24 4 24 WVE-004 PBS week 1.5 0.5 0.0 1.0 Relative Poly-GP levels (normalized to PBS)

ns Relative fold change C9orf72/HPRT1 1.5 0.5 0.0 1.0 WVE-004 PBS ns Relative fold change C9orf72/HPRT1 1.5 0.5 0.0 1.0 WVE-004 PBS Healthy C9orf72 protein relatively unchanged ~6 months after WVE-004 administration Neuro C9orf72

WVE-004: Adaptive SAD/MAD design to

optimize dose level and frequency Patients with documented C9orf72 expansion and confirmed ALS, FTD, or mixed phenotype (up to 50 patients planned) Starting dose informed by preclinical in vivo models Dose escalation and dosing interval guided by

safety committee Key biomarkers of target engagement and neurodegeneration will be assessed PolyGP NfL Key exploratory clinical outcome measures ALSFRS-R and CDR-FTLD Clinical trial site activation ongoing Dosing in Phase 1b/2a trial expected to

initiate in 2021 CTA: clinical trial application; NfL: neurofilament light chain; ALSFRS-R: Amyotrophic Lateral Sclerosis Functional Rating Scale; CDRFTLD: Clinical Dementia Scale - frontotemporal lobar degeneration;PolyG: poly

glycine-proline; SAD: Single ascending dose; MAD: Multiple ascending dose Neuro C9orf72

WVE-003 Huntington's

Huntington's disease mHTT toxic effects lead to neurodegeneration, loss of wtHTT functions may also contribute to HD Wild-type HTT is critical for normal neuronal function Expanded CAG triplet repeat in HTT gene results in production of mutant

huntingtin protein Huntington's disease affects entire brain Monogenic autosomal dominant genetic disease; fully penetrant Characterized by cognitive decline, psychiatric illness, and chorea; fatal disease Stresses wtHTT Stresses wtHTT mHTT +

~50% decrease in wtHTT Healthy CNS function Synaptic dysfunction | Cell death | Neurodegeneration Loss of wtHTT functions Neuro HD

Plays an essential role in the

transport of synaptic proteins-including neurotransmitters and receptors-to their correct location at synapses9-12 Promotes neuronal survival by protecting against stress (e.g., excitotoxicity, oxidative stress, toxic mHTT

aggregates)1-8 BRAIN CIRCUITS SYNAPSE NEURON CSF circulation Supplies BDNF to the striatum to ensure neuronal survival13-16 Regulates synaptic plasticity, which underlies learning and memory17-22 Plays a critical role in formation and function of

cilia-sensory organelles that control the flow of CSF-which are needed to clear catabolites and maintain homeostasis23 HD: Wild-type HTT is a critical protein for important functions in the central nervous system BDNF, brain-derived

neurotrophic factor; CSF, cerebrospinal fluid; mHTT, mutant huntingtin protein. Sources: 1. Leavitt 2006 2. Cattaneo 2005 3. Kumar 2016 4. Franco-Iborra 2020 5. Hamilton 2015 6. Ochaba 2014 7. Wong 2014 8. Rui 2015 9. Caviston 2007 10. Twelvetrees

2010 11. Strehlow 2007 12. Milnerwood 2010 13. Smith-Dijak 2019 14. Tousley 2019 15. Zhang 2018 16. McAdam 2020 17. Altar 1997 18. Zuccato 2001 19. Gauthier 2004 20. Ferrer 2000 21. Baquet 2004 22. Liu 2011 23. Karam 2015 Neuro HD

Cerebral cortex Striatum BDNF-

containing vesicle To the striatum Microtubule HTT HTT provides BDNF, a growth factor critical for survival of striatal neurons BDNF, brain-derived neurotrophic factor; HD, Huntington's disease; HTT, huntingtin protein. 1. Altar CA, Cai N,

Bliven T, et al. Nature. 1997;389(6653):856-860. 2. Zuccato C, Ciammola A, Rigamonti D, et al. Science. 2001;293(5529):493-498. 3. Gauthier LR, Charrin BC, Borrell-Pag s M, et al. Cell. 2004;118(1):127-138. 4. Ferrer I, Goutan E, Mar n C,

et al. Brain Res. 2000;866(1-2):257-261. 5. Baquet ZC, Gorski JA, Jones KR. J Neurosci. 2004;24(17):4250-4258. 6. Cattaneo E, et al. Nat Rev Neurosci. 2005;6(12):919-930. From the cerebral cortex Striatal neurons do not produce BDNF, but they need

it to survive1 HTT promotes the production of BDNF and transports BDNF from the cortex to the striatum2,3 In HD, decreased levels of BDNF contribute to degeneration of corticostriatal circuits2,4,5 Reduction of wtHTT may decrease the availability of

BDNF and accelerate corticostriatal degeneration6 Corticostriatal circuits Neuro HD

Target mutant mRNA HTT transcript to

reduce mutant HTT protein Preserve wild-type HTT protein reservoir in brain Allele-selective approach to treating HD Wave has only allele-selective clinical program in Huntington's disease Only an allele-selective approach is designed to

address both toxic gain of function and toxic loss of function drivers of HD Stresses wtHTT mHTT + Reduce Preserve Neuro HD

Nature publication contributes to

weight of evidence on importance of wild-type huntingtin Source: Poplawski et al., Nature, April 2019 Htt: Huntingtin protein Conditional knock-out of Htt in 4-month old mice (post-neuronal development) Results suggest that: Htt plays a central role

in the regenerating transcriptome (potentially influencing genes such as NFKB, STAT3, BDNF) Htt is essential for regeneration Indeed, conditional gene deletion showed that Htt is required for neuronal repair. Throughout life, neuronal maintenance

and repair are essential to support adequate cellular functioning Neuro HD

WVE-003 (SNP3) demonstrates

selective, potent, and durable reduction of mHTT in preclinical models Selectively reduces mHTT mRNA in HD iPSC neurons in vitro Results from ND50036 iPSC-derived medium spiny neurons. Total HTT knockdown quantified by qPCR and normalized to

HPRT1 Oligonucleotide or PBS [100 g ICV injections through a cannula on days 1, 3, and 5] delivered to BACHD transgenic. Mean SD (n=8, *P<0.0332, ***P<0.0002, ****P<0.0001 versus PBS unless otherwise noted). HPRT1,

hypoxanthine-guanine phosphoribosyl transferase; iPSC, induced pluripotent stem cell; ICV, intracerebroventricular; PBS, phosphate-buffered saline Similar results in cortex Pan-silencing reference compound WVE-003 PBS Weeks *** ****

**** **** **** **** Pan-silencing reference compound WVE-003 Percentage HTT mRNA Remaining Durable striatal mHTT knockdown for 12 weeks in BACHD mouse model Neuro HD Incorporates PN backbone chemistry modifications

PK-PD modeling to guide dosing in

clinical trial PK: pharmacokinetic PD: pharmacodynamic IC50: the concentration of observed half of the maximal effect mHTT: mutant huntingtin protein BACHD Ascending dose studies PK & mHTT knockdown data IC50 determination Concentrations in

cortex and striatum sufficient for target engagement NHP Anticipated mHTT knockdown in cortex and striatum Human (cortex, striatum) Neuro HD

WVE-003: Clinical trial to leverage