While mechanistic studies in animal models are limited, recent work in T1DM and T2DM mouse models demonstrated that AF promotion is related to pro-arrhythmic activation of CaMKII (due to oxidative stress-mediated oxidation and O-GlcNAcylation of CaMKII)124 that would potentially affect multiple ion currents.83 The gene discussed is CAMK2G; the disease is atrial fibrillation.