CASP3 and cancer: For instance, while genes coding for pro-apoptotic caspases (such as CASP8, CASP9 or CASP3) are under significantly heavy, loci-specific, negative selection or genetic deletion pressures within most human cancers (Figure 1); yet this is not always the case for necrosome-relevant genes (such as RIPK1, RIPK3 or MLKL), which experience random or unspecific genetic deletions at the same rate as background genetic aberration frequency in human cancers (Figure 1).