Altogether, these findings suggest that hyperglycemia increases cytoplasmic sodium and protons as well as decreases mitochondrial biogenesis and ATP production via SGLT2, which further indicates that hyperglycemia-induced SGLT2-dependent elevation of cytoplasmic sodium and protons could be a new pathogenesis for diabetic nephropathy [44–46]. The gene discussed is SLC5A2; the disease is diabetic kidney disease.