ENOX2 and neoplasm: Again, this could be associated with the absence of extramitochondrial oxidative stress derived from tNOX abrogation, which, unlike the two tumor types, allowed the HPDE6-E6E7 cell system to re-establish its redox homeostasis by endogenous antioxidant mechanisms without ceasing to experience some level of affectation at the level of complex III mediated by CAP.