In addition, fadraciclib was synergistic with the BCL2 antagonist, venetoclax, inducing more profound CLL cell death, especially in samples with 17p deletion.113 CDK9 bound to the MYCN-amplicon super-enhancer as a component of P-TEFb; therefore, fadraciclib suppressed MYCN transcription, leading to growth arrest and apoptosis. This evidence concerns the gene CDK9 and B-cell chronic lymphocytic leukemia.