HHIP and liver dysplastic nodule: Consistent with the notion that GEC injury may lead to podocyte damage, and that podocyte loss further exacerbates GEC injury, forming a vicious cycle ultimately leading to DN that has been gaining attention1–3, our data indicate that augmented Hhip gene expression is associated with podocyte transition from a normal morphology to an apoptotic and/or fibrotic-like phenotype, and are further supported by the finding that human HHIP is upregulated in glomerular cells, in patients with focal segmental glomerulosclerosis30.