Mice with epidermal keratinocyte-specific ablation of RIPK1 (RIPK1E-KO) develop severe skin inflammation mediated by RIPK3-MLKL-dependent keratinocyte necroptosis, which is strongly suppressed by ZBP1 deficiency but only partially ameliorated by TNFR1 knockout [6, 10]. This evidence concerns the gene MLKL and dermatitis.