The pathophysiology of psoriasis is correlated with the STAT3/IL-17A signaling pathway [4], with activated Th17 cells producing cytokines such as IL-17A, IL-21, and IL-22, which stimulate keratinocytes to produce antimicrobial peptides, promote the proliferation of keratinocytes, and inhibit the differentiation of keratinocytes. This evidence concerns the gene IL17A and psoriasis.