TIFAB Modulates Metabolic Pathways in KMT2A::MLLT3-Induced AML Through HNF4A

This study aims to investigate the role of TIFAB in regulating leukemia stem/progenitor cell (LSPC) metabolism and proliferation in KMT2A::MLLT3-induced acute myeloid leukemia (AML). Building upon our previous findings of elevated TIFAB expression in AMLs and its impact on oxidative phosphorylation (OXPHOS), we explore the effects of TIFAB deletion on LSPC function, metabolic pathways, and downstream targets. By identifying hepatocyte nuclear factor 4alpha (HNF4A) as a key mediator of TIFAB's effects on leukemia cell metabolism and proliferation, this study provides new insights into the metabolic regulation of leukemia biology. The findings underscore the crucial role of TIFAB in AML and may contribute to the development of novel therapeutic strategies targeting metabolic vulnerabilities in leukemia stem cells.