The overexpression of ENO1 significantly abrogated the CCDC65-mediated suppression of AKT1 pathway, N-cadherin, Vimentin, CCND1 and the stimulation of E-cadherin and P21 (Figure S4C), suggesting that ENO1 is involved in the CCDC65-regulated of AKT1 pathway in GC. The gene discussed is VIM; the disease is gastric cancer.