In glioma, tigecycline treatment significantly increases the expression of miR-199b-5p, which target hairy and enhancer of split homolog-1 (HES1), a basic helix-loop-helix transcriptional repressor served as a downstream target of the Notch signaling pathway [86], thereby inactivating PI3K/AKT through reducing AKT phosphorylation at position Ser473 [27]. The gene discussed is AKT1; the disease is central nervous system cancer.