sin (H&E) staining of the kidney was performed. Both WT and KO mice displayed tubular damage on days 1, 2, and 3 after renal IR injury, as evidenced by tubular dilatation/vacuolation, loss of the brush border, cast formation, tubular necrosis, and peritubular capillary congestion at the site of the renal cortex or corticomedullary junction (Fig 2A). Consistent with the renal dysfunction described