Given that damaged cell-derived self-RNA can stimulate TLR3 signaling, these findings imply that ΔNp63lo/- keratinocytes in AD lesions may cause chronic inflammation through a vicious cycle of their own TSLP-TSLPR axis loop induced by RNA moieties derived from surrounding damaged keratinocytes [15], [16]. This evidence concerns the gene TLR3 and Alzheimer disease.