AKT1 and cancer: Consistently, in either cancer cells or oral keratinocytes, AN mediates the EMT process by decreasing epithelial markers (E-cadherin, involucrin) and increasing mesenchymal markers (N-cadherin, vimentin) via activating the phosphoinositide-3-kinase–protein kinase B/Akt (PI3K-PKB/Akt) pathway [106,107].