The inability of Nec-1 to fully suppress IAP antagonist/CD95L-mediated necroptosis raised the possibility of a potential activation of the necroptotic signalling machinery downstream of RIPK1, as observed in other studies.30, 32 Therefore, we next studied the kinetics and extent of MLKL phosphorylation in the presence or the absence of cIAPs (Figures 4c and d) under conditions of necroptosis induction (zVAD/CD95L versus zVAD/IAP-antagonist/CD95L) in RIPK3-reconstituted melanoma cells. This evidence concerns the gene MLKL and melanoma.