The current hypothesis on the primary role of epidermal barrier impairment in initiating the immune abnormalities in AD includes the secretion of alarmins (IL-25, HMGB1, IL-33, IL-1 and TSLP) by damaged KCs [38], which in turn prime Langerhans cells (LCs) to initiate a local Th2 immune response [39,40,41]. The gene discussed is IL1A; the disease is Alzheimer disease.