Given that we previously found that conditional knockout of Sav1 in mouse renal tubule cells results in renal fibrosis upon acute kidney injury (AKI) with aristolochic acid (AA), concomitant with an oncogene-induced senescence phenotype25, next we went on to examine whether it is in part due to Sav1-deletion induced Akt hyperactivation. This evidence concerns the gene SAV1 and acute kidney injury.