Our research verified that under diabetic injury, the elevated miR-320, together with Ago2 and RNA Polymerase II, promotes CD36 transcription, while Ago2 stabilizes miR-320 throughout this process.[9] CD36 is a free fatty acid transporter on the surface of cardiomyocytes.[66] Elevated CD36 expression accelerates cardiomyocyte lipid deposition, contributing to the progression of diabetic cardiomyopathy by generating excessive ROS, altering metabolic balance, and promoting apoptosis.[67,68]. This evidence concerns the gene CD36 and diabetic cardiomyopathy.