Moreover, in diabetic mice, both genetic deletion of functional domain of KIM‐1 as well as pharmaceutical inhibition of KIM‐1 attenuated DKD kidney injury, by mediating palmitic acid‐bound albumin uptake; this indicated a potential therapeutic role of KIM‐1 inhibitors in DKD via regulating PTC fatty acid uptake.93 The gene discussed is HAVCR1; the disease is diabetic kidney disease.