For proximal renal tubules, the metabolic transition from FAO to glycolysis is mainly present in the failed repair population, signaling the disease progress.[51, 52] Our present study has identified FOXK1 as the key driver of glycolysis in TECs in the context of renal fibrosis, whether it is the same case for FOXK1 acts in AKI, another disease setting, needs further investigation. The gene discussed is FOXK1; the disease is acute kidney injury.