While mice with the overexpression of casepase-1 in keratinocytes will spontaneously develop dermatitis with high serum IL-18 level [80,81]; treatment with caspase-1 inhibitor or blocking IL-18, however, significantly mitigate the AD symptoms and reduce plasma thymic stromal lymphopoietin (TSLP) level in AD mice with or without UVB irradiation [37], which further implicated that NLRP3 inflammasome and its downstream players caspase-1 and IL-18 are paramount in both development and exacerbation of AD. This evidence concerns the gene NLRP3 and Alzheimer disease.