Diabetic mice with a podocyte-specific deletion of RBPj, which is essential for canonical Notch signaling, were partially protected against renal damage, exhibiting lower levels of albuminuria and less podocyte dedifferentiation and loss, accompanied by reduced TGF-β and vascular endothelial growth factor (VEGF) expression compared with wild-type mice with DN (Niranjan et al., 2008). Here, VEGFA is linked to liver dysplastic nodule.