HAVCR1 and diabetic kidney disease: Lipid accumulation is commonly observed in patients with DKD (31), which is supposed to be due to increased uptake of fatty acid through CD36 (32) and KIM-1 (33), enhanced fatty acid synthesis, and downregulation of FAO genes; however, this is the first report to our knowledge demonstrating that carnitine deficiency–induced impairment of FAO was associated with the decline in eGFR and tubular injury along with the increased ectopic lipid accumulation in the kidneys of patients with DKD.