While FADD deficiency or RIPK1 kinase-dead expression prevented hepatocyte cell death and development of liver disease in OTULINLPC-KO mice, genetic deletion of TNF or TNFR1 did not ameliorate the liver phenotype24, in sharp contrast with our observations in keratinocyte-specific OTULIN-deficient mice, where ablation of TNFR1 signaling resulted in a complete rescue of cutaneous inflammation. The gene discussed is OTULIN; the disease is liver disorder.