Thus, apoptotic extrinsic pathways involving TNFR/TRAIL-R as well as intrinsic pathways involving cytochrome c and AIF, through caspase dependent and independent mechanisms respectively via the mitochondria can all be abrogated by cancer cells in addition to their ability to alter expression levels and function of anti-apoptotic proteins such as Bcl-2 family members [41, 79-81]. The gene discussed is BCL2; the disease is cancer.