Lee et al. showed that empagliflozin treatment improved mitochondrial fragmentation and enhanced renal proximal tubule cell autophagic activity under hyperglycemia by involving the AMP-activated protein kinase (AMPK) and the mammalian target of rapamycin (mTOR) signaling pathways, resulting in reduced apoptosis and tubulo-interstitial fibrosis [50], so empaglifozin improved tubular mitochondrial dynamics and increased autophagic activity. This evidence concerns the gene MTOR and Hyperglycemia.