Considering that levels of reactive oxygen species (ROS) such as H2O2 and superoxide are elevated following myocardial infarction [14], we hypothesized that oxidation of CaMKII represents an important pathway for CaMKII activation in the infarct border zone (BZ) that may provide a mechanistic link between increased ROS production, Na+ channel remodeling and conduction slowing following MI. This evidence concerns the gene CAMK2G and myocardial infarction.