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To address this limitation, we employ a single-cell multiomic framework to functionally dissect common regulatory variants associated with B-ALL risk. Coupling this multiomic analysis with assessment of allelic skews in chromatin accessibility, we reveal the impact of risk alleles and disruptions in transcription factor networks specific to B-cell progenitors, thereby providing mechanistic insights into altered regulatory programs underlying B-ALL predisposition. By constructing long-range variant-to-target gene maps, we identify 34 high-confidence B-ALL susceptibility genes. Among these, we uncover and functionally validate a risk allele that selectively upregulates expression of\n                  <jats:italic>ELK3<\/jats:italic>\n                  , a previously unrecognized regulator of B-cell development and leukemogenesis. Together, these findings establish a comprehensive variant-to-function map of cell state-specific regulatory disruptions underlying inherited predisposition to B-ALL and define new risk mechanisms, which could pave the way for future targeted prevention approaches.\n                <\/jats:p>","DOI":"10.64898\/2026.08.06.743308","type":"posted-content","created":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T15:35:46Z","timestamp":1786116946000},"source":"Crossref","is-referenced-by-count":0,"title":["Single-cell multiomic mapping of genetic predisposition to childhood B-cell acute lymphoblastic leukemia"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9917-8834","authenticated-orcid":false,"given":"Andrew J.","family":"Lee","sequence":"first","affiliation":[{"name":"Division of Hematology\/Oncology, Boston Children\u2019s Hospital, Harvard Medical School, Boston, MA, USA"},{"name":"Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard 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