According to a literature review, miRs associated with AF might be regulated by ROS, suggesting that cellular stressors, such as ROS, may contribute to the development of AF [119]: ROS targets some key electrical remodeling-related molecules, such as CaMKII, RyR, LTCC, SERCA, and NCX, as well as an array of miRs with the potential to affect the arrhythmogenic process (e.g., targeting ion channels [108]): miR-Let-7e, -499, -1, -130a, -19, -145, -133, -328, -30, -23, and miR-21 to name the most prominent. This evidence concerns the gene CAMK2G and atrial fibrillation.