The cigarette-smoke-induced malignant transformation of bronchial epithelial cells , including characteristics of amplified colony formation, invasion and migration capacities, is dependent on HIF-1α-induced miR-21 upregulation, which subsequently inhibits phosphatase and tensin homolog (PTEN), a classic tumor suppressor, to activate the Akt/NF-κB pathway [51], while in gastric cancer cells, PTEN inhibition caused by HIF-1α-mediated miR-382 expression inversely restrains the Akt/mTOR signaling pathway, conferring miR-382 with angiogenic effects [52]. This evidence concerns the gene AKT1 and neoplasm.