Thank you, Allen. We have oriented Voyager to address some of the most critical challenges facing gene therapy, potentially unlocking the tremendous opportunity this modality holds to help patients. With first-generation AAV gene therapies, tissue-specific targeting is typically suboptimal, and the therapeutic index is often poor. As a result, many developers have encountered major toxicity issues if they dose high enough to achieve efficacious levels, with toxicity limiting the potential for optimal efficacy in many cases. In fact, a recent analysis revealed that clinical trials evaluating cell and gene therapies accounted for approximately 40% of all clinical holds in 2021. The ability to produce capsids capable of delivering a payload to specific tissues, whether that is for CNS or cardiac tissue or other parts of the body with limited exposure elsewhere is critical to the success of AAV gene therapy. We believe that Voyager has developed a core technology with our TRACER capsid platform that may enable meaningful therapeutic benefit for patients. TRACER allows us to evaluate millions of different possible modifications to existing AAV capsids, and select only those capsids to display increased transduction in specific tissues or cells. This approach takes advantage of 2 distinct methods that historically have not been used by others in this field. The first is to perform this initial screening, along with a series of subsequent screens in nonhuman primates, so that we're selecting for capsids that show enhancements in a species very closely related to humans, not those that have only shown activity in mice, which often don't translate well into human beings. Second, we measure the performance of our capsids at each step of the screening process by evaluating the expression level of messenger RNA or mRNA. In order to produce mRNA an AAV vector directed to a CNS target must pass through the blood-brain barrier, find the target cells in the brain or spinal cord, get through the cell membrane into the endosomes, get out of the endosomes, into the nucleus, produce double-stranded DNA and then produce mRNA. It's a very complicated process that we don't need to fully understand. Thus, when we measure production of the desired mRNA in the target tissue, we've got confidence that we are selecting capsids that not only get across the blood brain barrier, but they get into cells and deliver and express the payload productively. The TRACER approach has enabled us to identify and find capsids and surpass the delivery capabilities of the parental vectors that we're working with, including AAV9 and AAV5 by considerable margins in nonhuman primates and other animal species. An initial set of our proprietary AAV vectors from our first campaign to readout have demonstrated superior blood-brain barrier penetration enhanced cardiac muscle tropism and increased transgene expression in target tissues compared to conventional AAV capsids when dosed intravenously in nonhuman primates, which we believe are a much better model for projecting performance in humans than rodents. One of our AAV9 derived TRACER capsids from this first campaign achieved a more than 1,000-fold increase in transgene mRNA expression compared with AAV9. This initial effort also identified an additional capsid that has shown an enhanced tropism for cardiac tissue and de-targeting of the dorsal root ganglia compared to conventional AAV. More recently, a new set of tracer AAV9 variants have demonstrated the improved CNS targeting in both nonhuman primates and rodents, with certain capsids capable of exhibiting preferential tropism for glial cells. Achieving glial cell tropism in addition to the capsids that had been previously demonstrated neuroma tropism is important because it may enable more effective targeting of certain CNS diseases. We are performing further tracer screening campaigns to identify additional proprietary AAV9 and AAV5-derived capsids targeting multiple tissue and cell types inside and outside the CNS. In parallel, we are further refining the promising capsids already identified to enhance desirable characteristics for use in gene therapies to treat a broad range of diseases. We look forward to presenting more data from our expanding capsid library in the spring. We anticipate our advances in capsid development will have a direct impact on our ability to advance Voyager's programs. We believe we are well positioned to develop best-in-class programs, thanks to our proprietary TRACER capsids that may broaden the therapeutic windows needed to successfully treat diseases with serious unmet medical needs. We're focused on programs with the capacity for target validation and an early point in the development process, establishing more efficient path to preclinical and clinical proof of concept and the potential to provide meaningful therapeutic benefit. We believe our capsid may enable programs across our portfolio with systemic IV delivery that harnesses the full vasculature of the brain to reach desired cells while lowering the risk of dose-limiting toxicities. Our programs leveraging the TRACER capsids for IV delivery include gene replacement programs for spinal muscular atrophy and diseases linked to GBA1 mutations, including Parkinson's disease, Lewy body dementia and Gaucher disease. Knockdown programs for SOD1 ALS and Huntington's disease and vectorized antibody programs for HER2-positive breast cancer brain metastases and diseases associated with [indiscernible] pathology. In each of these areas, we believe that our approach has the potential to result in transformational new therapeutic approaches for patients facing devastating conditions. We expect to present preclinical data on some of our programs at the Spring Medical Conference. One example of the progress we are making is our presentation at last November Society for Neuro-Oncology Annual Meeting, where we shared positive preclinical data in mice on our IV administered vector including an anti-HER2 antibiotic payload to target HER2-positive brain metastases utilizing a TRACER AAV capsid. HER2-positive breast cancer patients with brain metastases face major unmet need. While approved anti-HER2 therapies are effective for peripheral disease, they have a limited ability to reach the CNS in sufficient concentrations to treat brain metastases. By using one of our proprietary CNS-targeted capsids to deliver a vectorized antibody payload and by utilizing cells within the brain to produce therapeutic antibodies, we've demonstrated a durable effect against CNS tumors in several mouse models. We believe our ability to make an impact for patients and create value extends beyond our own pipeline with the potential application of our TRACER capsids in our partners' programs. Our arrangements with partners provides the opportunity to enable new medicines, leveraging the substantial development knowledge and capabilities of these larger organizations. We believe that we'll be able to further expand our impact through additional partnerships. I'll now hand it over to Julie to review financial highlights.