It is widely accepted that the stratum corneum (SC) is dysfunctional in AD as a result of abnormal lipids (e.g., reduced ceramides and free fatty acids, an increase in unsaturated chain length) [4], altered expression of epidermal differentiation genes (e.g., loricrin, small proline-rich region proteins (SPRR)), filaggrin null-mutations, imbalance of proteases and protease inhibitors, and trauma from a chronic itch-scratch cycle (reviewed in [5]). The gene discussed is LORICRIN; the disease is Alzheimer disease.