Atrial fibrillation is thought to develop due to changes mediated by early and delayed after depolarization (EAD, DAD) events, and is linked to changes in gene expression including the dysregulation of RYR2, reduced sarcoplasmic/endoplasmic reticulum Ca2+-ATPase2 (SERCA2, encoded by ATP2A2), and increased Na+/Ca2+ exchanger (NCX) [37]. The gene discussed is TLX2; the disease is atrial fibrillation.