However, given that key electrical remodeling-related molecules, such as CaMKII, RyR, LTCC, SERCA and NCX, are targeted by ROS [80] and that an entire array of miRNAs with the potential to affect the arrhythmogenic process (i.e., targeting ion channels [108]) has not been investigated regarding any possible ROS-dependent regulation, the odds of the existence of such an ROS–miRNA–AF framework in the setting of arrhythmogenesis are reasonably high (Figure 1). The gene discussed is RYR2; the disease is atrial fibrillation.