IL-33, a major cytokine in the pathogenesis of AD, may reduce IL-37 through two pathways: (a) downregulating loricrin and filaggrin expression either directly or through IL-33-induced IL-4 and IL-13 downregulation, and subsequently downregulating IL-37 [171,172,173], or (b) stimulating keratinocyte production of chemokines such as CXCL1 and CXCL8, promoting neutrophil infiltration, and CCL20, facilitating Th17 cell recruitment [174]. The gene discussed is IL4; the disease is Alzheimer disease.