However, NHE-1 hyperactivity causes a high concentration of intracellular Na+ that accelerates sodium-calcium exchange and results in intracellular Ca2+ overload, leading to ventricular dysfunction, cardiac hypertrophy, apoptosis, and heart failure (Besse et al., 2004; Cingolani and Ennis, 2007). This evidence concerns the gene SLC9A1 and cardiac hypertrophy.