Li et al. [105] found that phloridzin increased NO output, suppressed SGLT1 and SGLT2 expression, and promoted the consumption of glucose, which ameliorated endothelial dysfunction by the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/endothelial nitric oxide synthase (eNOS) signaling pathway in palmitic acid-induced human umbilical vein endothelial cells. The gene discussed is AKT1; the disease is endothelial dysfunction.