When skin tissue receives stimulations, such as trauma, injury, infection, and medication, the stressed or damaged cells in prepsoriatic skins release autoantigens such as nucleic acids, cationic antimicrobial peptides/proteins (AMPs), ADAMTSL-5, and PLA2G4D, which activate DCs and then through IL-23 to activate Th17 cells [38]. The gene discussed is IL23A; the disease is infection.