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]. This evidence concerns the gene TNFRSF1A and cancer.