Venetoclax and the cyclin-dependent kinase (CDK) inhibitor alvocidib were found to act synergistically in venetoclax sensitive and resistant AML models, with alvocidib acting to decrease MCL-1 and increase pro-apoptotic proteins Bim and NOXA, thereby complementing the venetoclax mechanism of action (41). Here, MCL1 is linked to acute myeloid leukemia.