In a cisplatin-induced and cyclosporine-induced AKI model, paricalcitol may ameliorate cisplatin-induced renal injury by suppressing fibrotic, apoptotic, and proliferative factors via a mechanism that may include the inhibition of transforming growth factor beta-1 (TGF-β1), suppression of mitogen-activated protein kinase signaling (MAPK), and attenuation of p53-induced apoptosis [44,45]. Here, TGFB1 is linked to acute kidney injury.