The reactivation of Notch1 signaling in podocytes contributes to diabetic glomerulopathy, and its modulation can be achieved through the pharmacological inhibition of RAS (Koshizaka et al., 2012; Gagliardini et al., 2013; Gao et al., 2016), the standard therapy for CKD, including DN, and of Rho kinase, which mediates TGF-β-induced Jag1 expression in podocytes (Matoba et al., 2017) (Figure 3A). The gene discussed is JAG1; the disease is liver dysplastic nodule.