The ablation of canonical Notch signaling in keratinocytes by simultaneous deletion of both Notch1 and Notch2 or RBP-J resulted in defective skin barrier function and increased expression of TSLP, leading to the development of a severe AD-like skin phenotype in mice (Demehri et al., 2008; Dumortier et al., 2010). Here, RBPJ is linked to Alzheimer disease.