Specific lipid metabolic reprogramming in macrophages and its association with the excessive production of IL‐6/IL‐23 form a crucial bridge in Th17‐driven pathological processes.[28] Existing studies have confirmed that Th17 differentiation requires TGF‐β combined with IL‐6, and IL‐23 stabilizes its function.[48, 49] However, they have not clarified how NAFLD specifically drives the metabolic mechanisms of this cytokine environment in the kidneys. This evidence concerns the gene IL6 and metabolic dysfunction-associated steatotic liver disease.