In addition, the non-selective SGLT inhibitor phlorizin ameliorates the endothelial dysfunction link with the activation of the PI3K/AKT/eNOS signaling pathway and augmentation of the release of nitric oxide (NO) [27], and SGLT2i EMPA, and DAPA restores NO bioavailability by inhibiting reactive oxygen species (ROS) generation [28]. The gene discussed is AKT1; the disease is endothelial dysfunction.