Cotreatment of primary AML blasts and AML cell line xenografts with venetoclax and the PI3 kinase/mTOR inhibitor GDC-0980 also resulted in enhanced apoptosis, involving MCL-1 downregulation and Bax activation, suggesting that coadministration of PI3K and BCL-2 inhibitors may be effective in AML treatment (43). The gene discussed is MCL1; the disease is acute myeloid leukemia.