ROS can activate CaMKII via oxidative phosphorylation.Phosphorylation of the CaMKII-dependent Nav1.5 Ser571 site after I/R in isolatedmouse hearts, leads to an increased susceptibility to cardiac arrhythmias [34].Phosphorylation is the most well-documented post-transcriptional modification incardiac Nav1.5 channels. The gene discussed is SCN5A; the disease is cardiac arrhythmia.