Along with co-morbidities such as obesity, hypertension, and kidney disease, these effects can lead to subclinical myocardial dysfunction or HF with reduced or preserved ejection fraction.1,3,4 Until the development of SGLT2 inhibitors, glucose-controlling therapies for DM had a neutral or harmful effect in HF endpoints [32], [33], [34], [35], [36]. The gene discussed is SLC5A2; the disease is hypertensive disorder.