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This review highlights recent advances in experimental systems used to connect CHD-associated genes and variants to developmental mechanisms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Recent Findings<\/jats:title>\n                    <jats:p>In vivo mouse and vertebrate studies have refined models of early cardiogenic mesoderm formation, heart-field allocation, valve development, outflow tract morphogenesis, epicardial-myocardial interactions, and ventricular compaction. Parallel work on postnatal cardiac maturation highlights how RNA processing, metabolic remodeling, immune signaling, and non-myocyte populations influence cardiomyocyte maturation and regenerative competence, with implications for long-term outcomes in CHD survivors. Human pluripotent stem cell models provide complementary platforms for investigating gene functions: two-dimensional differentiation enables scalable, temporally controlled analysis of lineage commitment and cell-autonomous phenotypes, whereas organoids and other three-dimensional models introduce spatial organization, multicellular interactions, and tissue-level readouts. Genome editing, CRISPR screening, base and prime editing, regulatory-element assays, and inducible protein-depletion systems now allow increasingly precise and high-throughput characterization of coding and noncoding variants.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Summary<\/jats:title>\n                    <jats:p>Together, these advances are enabling a transition in CHD research from descriptive genomics to integrated, multi-model approaches that connect genetic variation to gene function, developmental mechanisms, and disease phenotypes.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s11936-026-01157-y","type":"journal-article","created":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:04:44Z","timestamp":1791273884000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Elucidating Gene Functions in Congenital Heart Disease"],"prefix":"10.1007","volume":"28","author":[{"given":"Sukanya","family":"Raghu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ankit K.","family":"Tamta","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanchita Sanchaya","family":"Dey","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed Imdhiyas Abdul","family":"Basheed","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aniqua Tasnim","family":"Chowdhury","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Swetansu K.","family":"Hota","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2636-7228","authenticated-orcid":false,"given":"Nathan J.","family":"VanDusen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,10,6]]},"reference":[{"issue":"12","key":"1157_CR1","doi-asserted-by":"publisher","first-page":"1132","DOI":"10.1161\/CIRCULATIONAHA.120.046822","volume":"142","author":"KN Lopez","year":"2020","unstructured":"Lopez KN, et al. 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