MCL1 and neoplasm: Since c-Myc is known to concomitantly induce cell proliferation and apoptosis, the significantly increased MCL-1 levels observed in HTATIP2-deficient A549 tumors is likely to contribute to the rapid tumor growth by increasing the threshold of c-Myc activity required for initiation of apoptosis which in turn facilitates c-Myc-stimulated cell proliferation [59,60].