Considering that Lats2 knockout can lead to increased YAP expression, inhibition of p53 does not completely resist the inflammatory or fibrotic aggravation from LATS2 deficiency, which might be the reason that even in the presence of PFT-α treatment, Lats2-CKO mice exhibited severe chronic kidney damage compared to Lats2-Ctrl mice, suggesting that LATS2 deficiency exacerbates incomplete repair of AKI via p53-independent mechanisms. The gene discussed is LATS2; the disease is acute kidney injury.