Interestingly, our results support the hypothesis that SGLT2i can exert beneficial effects in reversing cardiac damage by increasing the NAD +/SIRT1 pathway in HF [3, 16] and are consistent with literature data demonstrating both the downregulation of SIRT1 under high glucose conditions, likely due to the activation of SGLT2 via GLUT2/importin-α1/ HNF- α1 [43], as well as the physical interactions between SIRT1-SGLT2 [44]. The gene discussed is SLC2A2; the disease is hydrops fetalis.