Rahmani et al. [34] emphasized the role of PI3K/Akt-driven MCL-1 upregulation in AML chemoresistance, showing that treatment with venetoclax and the PI3K inhibitor GDC-0980 rapidly promoted BAX translocation, cytochrome c release from mitochondria, and apoptosis across diverse AML cell lines, along with inhibition of Akt/mTOR activity and decreased MCL-1 expression. The gene discussed is MCL1; the disease is acute myeloid leukemia.