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]. This evidence concerns the gene SLC5A2 and obesity disorder.