Furthermore,to better understand the underlying molecular mechanism of METTL14 in CRC, on the one hand, we found that METTL14 knockdown could elevate the expression of Vimentin and N-cadherin, and decrease the expression of E-cadherin, in other words, METTL14 knockdown facilitates EMT process in CRC, and this promption could be reversed by the depletion of SOX4, on the other hand, we noticed that loss of METTL14 could activate PI3K/Akt signaling, and this activation was abrogated by disruption of SOX4 in CRC. This evidence concerns the gene AKT1 and colorectal carcinoma.