SCN5A gene variants leading to reduced cardiac Na+ channel function have similarly been implicated in increased AF risks both in clinical situations (Olson et al., 2005, Darbar et al., 2008) and experimental studies in genetically modified Scn5a+/− murine hearts (Sabir et al., 2008, Kalin et al., 2010, Martin et al., 2011a, Martin et al., 2011b, Huang, 2017). The gene discussed is SCN5A; the disease is atrial fibrillation.