A more recent study examined the differential effects of oxidation and O-GlcNAcylation on AF, concluding that the loss of the oxidation site on CaMKII (M281/282) was sufficient to ablate AF susceptibility in mouse models of both type 1 and type 2 DM (Mesubi et al., 2020). This evidence concerns the gene CAMK2G and atrial fibrillation.