Single-cell transcriptomic studies have demonstrated that CLL cells progressing on venetoclax transitioned to an NFκBhigh state that promoted the transcription of the alternative anti-apoptotic member Mcl-1, which in turn took the lead of cell anti-apoptotic defense at the expense of Bcl-2 [15]. The gene discussed is MCL1; the disease is B-cell chronic lymphocytic leukemia.