CD36 and diabetes mellitus: Using acyl-PEG, CD36 was shown to be S-acylated on up to 4 cysteines in the heart, and others have shown that mutating these 4 cysteine residues located within the cytoplasmic tails of CD36 prevented translocation of the transporter to the membrane in response to physiological stimuli.6 Greater S-acylation of the CD36 pool and subsequent localization to the sarcolemma would increase the influx of FAs into the heart, fueling the increased FA oxidation and myocardial triglyceride content consistently demonstrated in both patients2,3 and animal models of diabetes.50,51