Because hyperglycemia can activate HNF-1 [30, 45] and increased ROS production is associated with diabetic cardiomyopathy, we hypothesized that upregulation of SGLT1 in cardiomyocytes in type 2 diabetes contributes to the pathophysiology of diabetic cardiomyopathy by increasing oxidative stress through EGFR-PKC-Nox2 dependent mechanisms. The gene discussed is PRRT2; the disease is diabetic cardiomyopathy.