This suggests that the inhibition of MDM2 could lead to acute kidney injury and due to incomplete healing contribute to development of chronic kidney disease.30 In our previous studies we showed that MDM2 in acute kidney injury promotes tubular injury in early postischemic phase via augmentation of NF-kB signaling and thus inflammation in p53-independent manner.10 Our present data document, that all renal anomalies due to MDM2 depletion in unchallenged tubular epithelial cells are dependent on p53 activity, as the defects completely disappeared when p53 was absent. The gene discussed is TP53; the disease is acute kidney injury.