Examination of the role of LUBAC selectively in skin homeostasis, via conditional deletion of HOIL-1 and HOIP in mouse keratinocytes (keratin 14 promoter), revealed the onset of lethal postnatal dermatitis at 4–6 days-of-age, which was partially attributable to exaggerated TNFR1-mediated apoptotic caspase-8 activity but largely RIPK1-independent [145]. The gene discussed is RIPK1; the disease is skin disorder.