In the immunopathogenesis of psoriasis, keratinocytes respond to triggers such as injury, infection, or cytokine stimulation, and produce chemokines (CXCL1, CXCLl2, CCL20), antimicrobial peptides (S100A7, S100A8, S100A9, S100A12), DEFB4a/DEFB2, CAMP/LL37, and other inflammatory factors attract and activate pathogenic T cells (T17, Th1 and Th22) and neutrophils [3]. The gene discussed is CAMP; the disease is infection.