CAV1 and hyperlipidemia: Endotheliumspecific Cav1 knockout male mice develop hyperlipidaemia irrespective of diet yet maintain endothelial performance; mechanistically, loss of Cav1 elevates NO, which Snitrosates CD36 at the same cysteines that accept palmitate, competitively blocking palmitoylation and membrane targeting, thereby curbing lipid uptake, foamcell formation and myocardial lipotoxicity [184].