However, Mesubi et al. reported that oxi-CaMKII and O-GlcNAcylation played critical but distinct roles in the mechanism for increased AF in diabetic mice, the RyR2 activated by oxi-CaMKII contributed to AF but the O-GlcNAcylation-induced AF was independent of CaMKII [11]. This evidence concerns the gene CAMK2G and atrial fibrillation.