Previous research found that HNF3α prevented the apoptosis of podocytes and helped to mitigate the progression of diabetic nephropathy,[21, 22] and that it attenuate ferroptosis in HK‐2 cells under high‐glucose conditions.[23] Furthermore, the expression of this protein is greater in sepsis‐induced AKI,[19, 20] and it can also exacerbate the severity of radiation‐induced AKI.[24] However, the effect and mechanism of HNF3α on the progression from AKI to CKD remain underexplored. The gene discussed is FOXA1; the disease is acute kidney injury.