This scenario was later confirmed by reports showing that OTULIN deletion in the liver causes TNFR1-driven, apoptosis- and compensatory proliferation-mediated liver pathology, while OTULIN deletion in keratinocytes causes TNFR1-driven, RIPK1 kinase activity-mediated, cell death-dependent skin inflammation [65,66] (Table 1). This evidence concerns the gene OTULIN and dermatitis.