It is important to note that patients with AS exhibit a metabolic shift from fatty acid to glucose metabolism, which is characterized by a decreased expression of fatty acid translocase (FAT/CD36) protein, together with a downregulation of other fatty acid transporters, such as plasma membrane and heart-type cytosolic fatty acid binding proteins (FABPpm and H-FABP), β-oxidation, Krebs cycle, and oxidative phosphorylation proteins. Here, CD36 is linked to aortic valve stenosis.