Because tumor cells can become resistant to ABT-737 or ABT-199 upon treatment by upregulating Mcl-1 and Bcl2A1 [30,31,32], next-generation small molecule inhibitors that target selectively Bcl2A1, Mcl-1 [33], and Bcl-B—or act as pan-Bcl-2 family inhibitors [34,35]—are highly desirable for future apoptosis-based cancer therapeutics [27]. Here, MCL1 is linked to neoplasm.