Forward-Looking Statements This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. We intend such forward-looking statements to be covered by the

Corporate Presentation January 2023

Forward-Looking Statements This

presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. We intend such forward-looking statements to be covered by the safe harbor provisions for forward-looking statements

contained in Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. All statements contained in this presentation that do not relate to matters of historical fact should be

considered forward-looking statements, including, without limitation, statements regarding: our expectations surrounding the potential, safety, efficacy, and regulatory and clinical progress of our product candidates; the potential of our gene

therapy and gene editing platforms, including our GTx-mAb platform; our plans and timing for the release of additional preclinical and clinical data; our plans to progress our pipeline of genetic medicine candidates and the anticipated timing for

these milestones; our expectations surrounding our relationship with Oxford Biomedica Solutions; our competitive position, business strategy, prospective products, timing, design, results and likelihood of success of studies and/or clinical trials;

our position as a leader in the development of genetic medicines; and our plans to engage in future collaborations and strategic partnerships. The words "believe," "may," "will," "estimate,"

"potential," "continue," "anticipate," "intend," "expect," "could," "would," "project," "plan," "target," and similar expressions

are intended to identify forward-looking statements, though not all forward-looking statements use these words or expressions. These statements are neither promises nor guarantees, but involve known and unknown risks, uncertainties and other

important factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements, including, but not limited to,

the following: the impact of the COVID-19 pandemic on our business and operations, including our preclinical studies and clinical trials, and on general economic conditions; we have and expect to continue to incur significant losses; our need for

additional funding, which may not be available; failure to identify additional product candidates and develop or commercialize marketable products; the early stage of our development efforts; potential unforeseen events during clinical trials could

cause delays or other adverse consequences; risks relating to the regulatory approval process; interim, topline and preliminary data may change as more patient data become available, and are subject to audit and verification procedures that could

result in material changes in the final data; our product candidates may cause serious adverse side effects; inability to maintain our collaborations, or the failure of these collaborations; our reliance on third parties, including for the

manufacture of materials for our research programs, preclinical and clinical studies; failure to obtain U.S. or international marketing approval; ongoing regulatory obligations; effects of significant competition; unfavorable pricing regulations,

third-party reimbursement practices or healthcare reform initiatives; product liability lawsuits; securities class action litigation; failure to attract, retain and motivate qualified personnel; the possibility of system failures or security

breaches; risks relating to intellectual property; and significant costs incurred as a result of operating as a public company. These and other important factors discussed under the caption "Risk Factors" in our Quarterly Report on Form

10-Q for the quarter ended September 30, 2022 and our other filings with the Securities and Exchange Commission could cause actual results to differ materially from those indicated by the forward-looking statements made in this presentation. Any

such forward-looking statements represent management's estimates as of the date of this presentation. While we may elect to update such forward-looking statements at some point in the future, we disclaim any obligation to do so, even if

subsequent events cause our views to change. This presentation also includes statistical and other industry and market data that we obtained from industry publications and research, surveys and studies conducted by third parties or us. Industry

publications and third-party research, surveys and studies generally indicate that their information has been obtained from sources believed to be reliable, although they do not guarantee the accuracy or completeness of such information. All of the

market data used in this presentation involves a number of assumptions and limitations, and you are cautioned not to give undue weight to such estimates. While we believe these industry publications and third-party research, surveys and studies are

reliable, we have not independently verified such data. The industry in which we operate is subject to a high degree of uncertainty, change and risk due to a variety of factors, which could cause results to differ materially from those expressed in

the estimates made by the independent parties and by us.

Homology is a Leader in Genetic

Medicines, Developing One-Time, Potentially Life-Changing Therapies for Patients, Caregivers and Families By leveraging Homology's AAV technology, including our exclusive AAVHSC platform, we aim to: Deliver best-in-class gene editing therapies

by utilizing homologous recombination-based integration Replace chronic therapies with one-time GTx-mAb treatments Advance gene therapy with targeted capsid selection coupled with optimized design Pursue strategic partnerships to

progress and expand the platform

Fully Integrated Gene Therapy and Gene

Editing Company With Clinical Programs Rare Disease Experience Team's prior experience includes developing and/or launching 11 rare disease drugs with >$2B in annual revenue Technology 15 novel AAVHSCs; potential to expand Equity

investments from Pfizer and Novartis Extensive I.P. portfolio AAV Process Development and Manufacturing Expertise Co-owned Manufacturing and Innovation Business, Oxford Biomedica Solutions Research and Development Phase 1 gene editing in PKU Phase 1

gene therapy in Hunter syndrome Phase 1/2 gene therapy in PKU Discovery, Research & Development 5 development candidates

Flexible AAVHSC Platform Designed to

Address Rare Genetic Disorders and Diseases With Larger Patient Populations Promoter Corrective Gene Enters the Cell's Nucleus Promoter-Driven Tx-mAb Enters the Cell's Nucleus Episome with Promoter + Tx-mAb DNA mRNA Tx-mAb Continuous +

Sustained Systematic mAb Levels Homology Arm Homology Arm Corrective Gene Enters the Cell's Nucleus Episome with Promoter & Corrective Gene Mutated Gene mRNA Mutated Protein Mutated Gene Homologous Recombination Functional Gene mRNA

Protein Gene Therapy (Adds a Gene) Gene Therapy (GTx-mAb) Gene Editing (Nuclease-Free)

Homology's In Vivo AAVHSC Genetic

Medicines Pipeline Indication Research Preclinical Phase 1 Phase 2 Phase 3 Gene Editing (Nuclease-Free) Adult/Pediatric Phenylketonuria (PKU) Human Stem Cells Gene Therapy Adult PKU MPS II (Hunter syndrome) Metachromatic Leukodystrophy (MLD)

Partnering Opportunity GTx-mAb Platform Paroxysmal Nocturnal Hemoglobinuria (PNH) Undisclosed Ophthalmic Target HMI-103 - Ph 1 Trial in Adults HMI-102 - Ph 1/2 Trial* HMI-203 - Ph 1 Trial HMI-204 HMI-104 *Paused enrollment

Gene Editing Candidate HMI-103 for

Effective PKU Treatment Remains a High

Unmet Medical Need Phe target levels: Vockley J et al. Genetics in Medicine 2014; Levy H et al. Molecular Genetics and Metabolism 2019; van Spronsen FJ et al. Lancet Diabetes Endocrinol 2017. PKU is One of the Largest Established Rare Disease

Commercial Markets Only ~10% of Patients Treated With a Therapeutic Global Market: 50K pts 1-1.5K incidence U.S. Market: 16.5K pts 350 incidence Inborn error of metabolism caused by variants in PAH gene Results in loss of function of

phenylalanine hydroxylase responsible for metabolism of phenylalanine (Phe) If untreated, toxic levels of Phe accumulate and result in progressive and severe neurological impairment PKU Onerous low-Phe diet has poor compliance Diet not sufficient to

reduce Phe levels to recommended targets Approved therapeutics do not reconstitute normal biochemical pathway for ~95% of patients; all require chronic dosing Physicians, patients seek new treatment options Unmet Need

HMI-103: AAVHSC-Mediated Gene Editing

Inserting a Promoter and Functional PAH Gene at the Target Location 2 copies of non-functional PAH gene Non-functional mRNA Non-functional PAH enzyme PAH gene and liver-specific promoter flanked by homology arms Functional PAH enzyme Homologous

recombination Integrated, functional PAH gene using liver-specific promoter HMI-103 Functional mRNA Functional PAH enzyme Episome with PAH gene and liver-specific promoter Functional mRNA Integrated Promoter and Gene Provide PAH Expression

Integration knocks out mutated allele Potential for long-term correction Reduces non-functional PAH Episomes Provide PAH Expression Designed to maximize PAH expression in all transduced liver cells

Preclinical Data Supported

Advancement of HMI-103 Into Clinical Trials Similar mRNA Expression and On-Target Integration Observed in Both Murine and Humanized Models mRNA Expression On-Target Integration HMI-103 in Humanized Liver Murine Model Sustained Normalization of Phe

in Pahenu2 Model of PKU Long-Read Sequencing Method Surveyed Entire Genome No De Novo Mutations at Integration Site No Off-Target Integrations mRNA/10 ng RNA

Optimization of Gene Editing

Candidate HMI-103 Increased In Vivo Potency in Murine enu2 Model Potency Consistent Across all Timepoints Tested Reduction in Phe Dose (vg/kg) HMI-103 optimization included: vector and homology arms design, integration of promoter, packaging, etc.

HMI-102 Murine surrogate of HMI-103 Gene Editing Vector 10X More Potent than Gene Therapy Vector in Murine PKU Model Studies Conducted in Murine Pahenu2 Model Analysis compared dose at which 50% Phe reduction was achieved in Pahenu2 model

The pheEDIT Clinical Trial with

HMI-103 in Adults with PKU

pheEDIT Phase 1 Trial Evaluating

Investigational HMI-103 Gene Editing Candidate for PKU Dose 3 Dose 2 Cohort 2 n = up to 3 Dose 1 Cohort 1 n = up to 3 Cohort 3 n = up to 3 Dose-escalation trial evaluating safety and efficacy of single I.V. administration of HMI-103 in adults with

uncontrolled classical PKU 82-day screening / run-in period to assess pre-treatment Phe levels over time Stagger between patient dosing Prophylactic, steroid-sparing immunosuppressive regimen, including T-cell inhibitor (tacrolimus)

T-Cell Inhibitor with Steroids

Reduced Anti-AAVHSC nAb Response and Increased mRNA Expression in Non-Human Primates Increased mRNA Expression Reduced nAb Response Dexa = Dexamethasone Tacro = Tacrolimus Prophylactic Immunosuppression Regimen with T-Cell Inhibitor Tacrolimus and

Shorter Course of Steroids Being Utilized in pheEDIT and juMPStart Clinical Trials * P 0.05 *** P 0.001

pheEDIT Trial Objectives Evaluate

Safety and Tolerability of HMI-103 Evaluate Preliminary Efficacy: Effect on Phe Levels Primary Objectives Effect of Phe Levels at Different Timepoints, Dietary Intake Secondary Objectives Exploratory Objectives Additional Biomarkers

Participant Recently Dosed in

pheEDIT Trial, and Initial Data Expected Mid-Year First participant recently dosed; additional participants in screening Nine clinical sites, including key PKU KOLs More sites expected to be initiated Initial trials in adults with plans for younger

patients once safety and efficacy established in adults pheEDIT Initial Clinical Data Expected Mid-Year 2023

Gene Therapy Candidate HMI-203 for

High Unmet Need for Hunter Syndrome

Treatment That Addresses Peripheral and Cognitive Effects *WORLDSymposium 2022. Haroldson J, et al. *National MPS Society. "A Guide to Understanding MPS II." Patients on existing ERT continue to experience: Increased mortality,

sleep apnea, chronic and joint pain, lung and cardiac conditions, hearing loss, limited mobility/range of motion Anxiety caused by uncertainty of disease progression Shortened life expectancy ERT does not cross blood-brain-barrier (BBB);

Neuronopathic patients experience**: Decreased cognitive function, seizures, cerebrospinal fluid accumulation, carpal tunnel syndrome Life expectancy into the second decade Caused primarily by IDS gene mutations Leads to toxic lysosomal

accumulation of glycosaminoglycans (GAGs) Severe form includes progressive debilitation and intellectual decline followed by death in 10-20 years Prevalence: 1 in 100,000 to 1 in 170,000; primarily males MPS II (Hunter syndrome) All People

with MPS II Experience Peripheral Disease Manifestations

HMI-203: Homology's In Vivo

Gene Therapy Approach to Hunter Syndrome in juMPStart Trial One-time, in vivo gene therapy candidate Designed to deliver functional copies of IDS gene to peripheral organs and central nervous system (CNS) First systemic gene therapy to be evaluated

in clinical trial for Hunter syndrome I2S enzyme made and continuously expressed by the liver Promoter IDS Gene Episome with Promoter & IDS Gene Enters the Cell's Nucleus Non-Functional IDS Gene mRNA Non-Functional I2S Protein I2S Protein

Leads to Cross-Correction HMI-203

Glycosaminoglyan Heparan Sulfate

(GAG-HS) ( g/mL) HMI-203 Demonstrated Biochemical and Phenotypic Correction in MPS II Murine Model * p>0.05; ** p>0.01; *** p>0.001; "ns" = no significance. ASGCT 2021 and WORLDSymposium 2022. Smith, et al.

Biochemical Correction Phenotypic Correction HMI-203 Tissue GAG-HS (at 52 Weeks) Paw and Ankle Width CSF GAG-HS Levels (at 12 Weeks) Glycosaminoglyan Heparan Sulfate (GAG-HS) ( g/mL) WT - Vehicle MPS II - Vehicle MPS II - HMI

203 - Dose A MPS II - HMI 203 - Dose B MPS II - HMI 203 - Dose C MPS II - Vehicle MPS II - HMI-203 WT - Vehicle Zygomatic Arch Width

The juMPStart Clinical Trial with

HMI-203 in ERT-Treated Adults with Hunter Syndrome

juMPStart Phase 1 Trial Evaluating

Investigational HMI-203 Gene Therapy Candidate for Hunter Syndrome Dose 3 Dose 2 Cohort 2 n = up to 3 Dose 1 Cohort 1 n = up to 3 Cohort 3 n = up to 3 Dose-escalation trial evaluating safety and efficacy of single I.V. administration of HMI-203 in

ERT-treated adults with Hunter syndrome Stagger between patient dosing Prophylactic, steroid-sparing immunosuppressive regimen, including T-cell inhibitor (tacrolimus) ERT = Enzyme replacement therapy

juMPStart Trial Objectives Evaluate

Safety and Tolerability of HMI-203 Evaluate Preliminary Efficacy: Effect on MPS II Biomarkers Primary Objectives Evaluate Biomarkers, Functional Measures, Use of ERT Secondary Objectives Exploratory Objectives Evaluate Joint Range of Motion;

Quality-of-Life Assessments

juMPStart Initial Clinical Data

Expected 2H 2023 juMPStart Initial Clinical Data Expected 2H 2023 5 clinical sites in U.S. and Canada, including key Hunter syndrome KOLs More sites expected to be initiated Initial trials in adults with plans for younger patients once safety

and efficacy established in adults

Pipeline Updates and 2023

In Vivo GTx-mAb Candidate, HMI-104,

for the Treatment of PNH PNH Caused by Variants in PIGA gene Results in intravascular hemolysis (red blood cell destruction) caused by uncontrolled activation of complement system Chronic dosing with anti-C5s imperfect; patients struggle with:

Fatigue Anemia (~25%) Repetitive infusions (~25%) Hospitalizations Infection risk HMI-104

HMI-104 GTx-mAb Development