The pathophysiology of AD is complex and results from impaired epidermal barrier function and cutaneous inflammation as well as a type 2 helper T (TH2)-skewed immune dysregulation with elevated serum immunoglobulin (Ig)E level and peripheral blood eosinophilia, caused by the interaction between genetic and environmental predispositions (10–15). The gene discussed is IGHE; the disease is Alzheimer disease.