ZBP1 and dermatitis: Consistent with our earlier findings that ubiquitous TNFR1 deficiency delayed but could not prevent skin inflammation in FADDE-KO mice, Faddfl/flTnfr1fl/flK14-Cre Zbp1-/WT (hereafter referred to as FADDE-KO TNFR1E-KOZbp1−/WT) mice, which lack FADD and TNFR1 specifically in epidermal keratinocytes and are heterozygous for the Zbp1 knockout allele, developed progressive skin lesions between 3–10 weeks of life that reached pre-determined termination criteria requiring the humane sacrifice of the animals by the age of 11 weeks (Fig. 2A, B).