It was worth noting that the repression of LUBAC component HOIL1 or HOIP enhanced TNF-induced necroptosis.47 Similarly, the mutation of Sharpin led to TNF-dependent inflammatory syndrome, characterized by dermatitis, liver inflammation, splenomegaly and loss of Peyer's patches.48 Although loss of a single allele of Casp8 was strikingly effective in delaying the onset of dermatitis, it did not have an impact on other aspects of phenotype. Here, TNF is linked to dermatitis.