To investigate which of the pathways play significant roles in nephroprotection against AKI in αMUPA mice, and the involvement of uPA overexpression in this phenomenon, we applied both an in vivo model of AKI in these mice and an in vitro platform where the impact of the uPA treatment was examined in the HEK-293 and ACE-2 overexpressing cells. The gene discussed is PLAU; the disease is acute kidney injury.