Both spontaneous and IAP antagonist/DL-mediated MLKL phosphorylation following necroptosis induction is blocked in the presence of specific RIPK3 inhibitors.24 These data demonstrate (a) the functionality of RIPK3 for activation of its downstream target within the necroptotic signalling machinery and (b) the requirement of the kinase function for this phosphorylation event in melanoma cells. The gene discussed is RIPK3; the disease is melanoma.