In this in vivo study, mice were treated with ASA, GA, and TR (triciribine, the inhibitor of Akt activation) without or with heat stress, for evaluating our hypothesis that heat stress-induced acute kidney injury originated from peroxidation, and that Hsp90 enhanced cellular protection by restricting apoptosis and inducing autophagy-mediated survival by two separate signaling pathways, Hsp90-PKM2-Akt and Hsp90-HIF-1α-BNIP3/BNIP3L. This evidence concerns the gene HIF1A and acute kidney injury.