demonstrated that KHK is required for fructose‐mediated metabolic syndrome, TG formation, and hepatic steatosis in mice, and which endogenous fructose production and KHK activation within the kidney promotes the development of diabetic nephropathy and also reported for the first time that blockade of KHK may be an excellent treatment for the prevention and treatment of hereditary fructose intolerance. This evidence concerns the gene KHK and Hepatic steatosis.