A variety of pathological conditions, such as ischemia and hypoxia (Saint, 2006), cardiac hypertrophy and heart failure (Valdivia et al., 2005; Guo et al., 2014), can increase INaL, resulting in an elevated intracellular sodium concentration ([Na+]i), as well as a subsequent increase in the intracellular Ca2+ concentration ([Ca2+]i) as a result of the activity of a reverse Na+/Ca2+ exchanger (NCX), leading to Ca2+ overload resulting in arrhythmia (Kihara and Morgan, 1991; Haigney et al., 1992; Yeh et al., 2008; Tang et al., 2012). This evidence concerns the gene TLX2 and cardiac arrhythmia.