Meanwhile, the appropriate GCs have been reported to ameliorate acute kidney injury induced by renal ischemia–reperfusion injury [18] and reduce proteinuria by inhibiting the focal adhesion kinase (FAK)/receptor activator of nuclear factor-κB ligand (RANKL)/mitogen-activated protein kinase (MAPK) and FAK/RANKL/nuclear factor κβ (NF-κB) signaling pathways in rats with adriamycin-induced nephropathy [19]. Here, PTK2 is linked to acute kidney injury.