Since in most AD patients the skin shows superficial S. aureus colonization and barrier disruption due to reduction of ceramide or filaggrin (26, 27), bacterial products such as staphylococcal enterotoxins, lipoteichoic acid and peptidoglycan would likely penetrate the skin and induce the production of Th2 cells, and in turn Th1 cells and related chemokines, leading to a Th2 immune response and a subsequent Th1 immune response, thus augmenting skin inflammation (6, 10, 11, 14, 28). The gene discussed is FLG; the disease is Alzheimer disease.