Previous experimental and clinical data have shown that SGLT2 inhibitors cause a reduction in preload by promoting natriuresis and diuresis, thus the consequent reduction in cardiac dilation and remodeling.[17] Moreover, in the nondiabetic porcine model of HF, it has been found that SGLT2 inhibitors significantly ameliorated adverse anatomical LV remodeling and enhanced LV systolic function. The gene discussed is SLC5A2; the disease is hydrops fetalis.