Cav-1 was dissociated from caveolae to the cytosol in rat hearts after myocardial infarction (Ratajczak et al., 2003), which increased cytosolic Cav-1/endothelial NOS (eNOS) complexes, and subsequently, decreased the production of NO, a molecule to limit deleterious effects of ROS (Ratajczak et al., 2003). The gene discussed is CAV1; the disease is myocardial infarction.