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The present study systematically investigated the biological role of\n                    <jats:italic>DHCR7<\/jats:italic>\n                    in AML pathogenesis. In\u00a0vitro functional assays demonstrated that either\n                    <jats:italic>DHCR7<\/jats:italic>\n                    knockdown or treatment with the targeted inhibitor tamoxifen significantly suppressed AML cell proliferation. These inhibitory effects were accompanied by reduced intracellular cholesterol levels, accumulation of 7\u2010dehydrocholesterol (7\u2010DHC) and induction of endoplasmic reticulum stress, which ultimately triggered cellular apoptosis. Consistent with in\u00a0vitro findings, both\n                    <jats:italic>DHCR7<\/jats:italic>\n                    knockdown and intraperitoneal administration of tamoxifen markedly inhibited leukaemia progression in\n                    <jats:italic>NSG<\/jats:italic>\n                    (NOD Scid Gamma) mouse models, as validated by decreased bioluminescence intensity and reduced Ki\u201067 positivity. Mechanistic investigations further revealed that\n                    <jats:italic>DHCR7<\/jats:italic>\n                    exerts pro\u2010leukaemic effects through activation of the IL\u20106\/JAK2\/STAT3 signalling axis. Collectively, this study establishes the novel function of\n                    <jats:italic>DHCR7<\/jats:italic>\n                    in AML pathogenesis and provides robust evidence supporting its potential as a therapeutic target for AML.\n                  <\/jats:p>","DOI":"10.1111\/bjh.70346","type":"journal-article","created":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T10:44:50Z","timestamp":1769683490000},"page":"1263-1277","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["<scp>DHCR7<\/scp>\n                    drives\n                    <scp>AML<\/scp>\n                    development through the\n                    <scp>IL6<\/scp>\n                    \/\n                    <scp>JAK2<\/scp>\n                    \/\n                    <scp>STAT3<\/scp>\n                    signalling 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