Instead, lesions accumulating in cancers (loss-of-function mutations of the pro-apoptotic BAX and BAK1 genes, over-expressions of the anti-apoptotic Bcl-2 and Bcl-XL proteins, up-regulation of IAP family members, and post-translational modifications of Caspase-8) over their developmental phase, frequently interfere with the ability of Caspase-8 to execute apoptosis [10, 14–23]. The gene discussed is CASP8; the disease is cancer.