In conclusion, our observations indicate that the IL-17D–CD93-mediated decrease in DDX5 expression amplifies cutaneous inflammation and suggest a potential for IL-17D and DDX5 as therapeutic targets in inflammatory skin diseases, whereas the identification of sIL-36R provides insights into the contribution of aberrant RNA splicing to skin inflammation, and may ultimately lead to the development of alternative therapeutic approaches in AD and psoriasis. The gene discussed is CD93; the disease is Alzheimer disease.