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). This evidence concerns the gene MLKL and cancer.