The main perturbations in AF electrical remodeling leading to aberrant Ca2+ handling and resultant increased likelihood of reentry (Liu et al., 2020) and delayed afterdepolarization (a well-known trigger of AF) include persistent diastolic ryanodine receptor (RyR2) leak due to both sustained sarcoplasmic reticulum Ca2+ overloading, Ca2+/calmodulin kinase type II (CaMKII) activation, and upregulation of NCX (Nattel and Dobrev, 2012). Here, RYR2 is linked to atrial fibrillation.