Interestingly, in these patients’ group, venetoclax performs similarly to chemotherapy; it is therefore likely that the absence of a functional p53 translates into a critical lack of an important regulatory pathway of the apoptotic process, thus limiting the significance of BCL2 inhibition, as observed in studying interactions between ABT-737-induced apoptosis and chromosome 17 deletion in CLL cells [24]. The gene discussed is TP53; the disease is B-cell chronic lymphocytic leukemia.