Since AML cells have increased mitochondrial mass and oxygen consumption, Hurrish et al. have observed that dual inhibitor of PI3K and histone deacetylase (HDAC), named CUDC-907, when used in combination with Venetoclax (BCL-2 inhibitor), suppressed oxidative phosphorylation and mitochondrial function, causing cell death in both cytarabine-sensitive and -resistant AML cells [67]. This evidence concerns the gene PIK3CD and acute myeloid leukemia.