This is in agreement with the phenotype in Sharpincpdm/cpdm mice that also do not develop skin inflammation in the absence of TNFR1 or RIPK1 kinase signaling30,31, but is in contrast to the phenotype of keratinocyte-specific HOIP or HOIL-1 knockout mice that only show a delayed dermatitis in TNFR1 deficient or RIPK1 kinase-dead conditions8. This evidence concerns the gene RIPK1 and skin disorder.