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 skin disorder.