CD36 and myocardial infarction: In a murine model of acute myocardial infarction, AAV9mediated overexpression of a depalmitoylationdeficient CD36 mutant, as well as pharmacological inhibition of palmitoylation with SSO or 2bromopalmitate, improved ejection fraction and reduced infarct size, confirming that CD36 Spalmitoylation underlies postinfarction remodeling [12].