Given that upregulation of MCL-1 has been documented as a mechanism of resistance to the BCL-2 specific inhibitor venetoclax, and that other CDK inhibitors with activity against CDK9 have been shown preclinically to enhance the anti-tumor effects of BCL-2 inhibition, we next assessed whether systemic administration of the combination of voruciclib and venetoclax causes significantly enhanced tumor growth inhibition versus exposure to either single agent alone. Here, MCL1 is linked to neoplasm.