The possible mechanism of the protective effect of SGLT2 inhibitors on HF includes improvement of mitochondrial energy utilization, the restoration of renal tubular–glomerular feedback with resultant attenuation of renin–angiotensin II–aldosterone activation, diuretic and natriuretic effects, a decrease in sympathetic tone, improvement of mitochondrial calcium homeostasis, and a reduction in myocardial inflammation, oxidative stress, and fibrosis. The gene discussed is AGT; the disease is hydrops fetalis.