As the clinical development of navitoclax has been halted because of observed hematologic toxicity (30, 31), next-generation BH3-mimetic drugs in development include WH244, a proteolysis targeting chimera (PROTAC) that is specifically activated to degrade BCL-XL in tumor cells but not in platelets (56), and pelcitoclax, a small-molecule direct BCL-XL inhibitor (57). This evidence concerns the gene BCL2L1 and neoplasm.