Recently, authors have confirmed the involvement of the HGF/cMet pathway in kidney fibrosis and verified that the administration of a cMet agonistic Ab reduces fibrosis in primary cultured glomerular endothelial cells (GEnCs)11 and proximal tubular epithelial cells (PTECs) and improves fibrosis and apoptosis in a unilateral ureteral obstruction model.12 Here, MET is linked to Ureteral obstruction.