Mechanistically, the three inhibitors in combination more significantly inhibit HOXA9, MEIS1, and BCL2 expression and reduce pFLT3 levels [195], which are elevated in patient-derived MLLr and NPM1/FLT3 mutant AML cells that develop resistance to the combination of VTP50469 and venetoclax treatment [192]. The gene discussed is NPM1; the disease is acute myeloid leukemia.