TP63 and Alzheimer disease: GR loss-of-function achieved via stable GR knockdown (GRKD) in primary human keratinocytes resulted in AD-like features of HEEs including hyperplasia and abnormal differentiation, constitutive increases in P63, upregulation of disease markers, and increased autocrine production of TH2-/TH1-/TH17-TH22-associated factors, relative to controls.