In summary, our work confirmed Li's study that METTL3, a critical m6A methyltransferase, could facilitates CRC progression, and further revealed a new mechanism that METTL3 could promote CRC cells proliferation by directly stabilizing CCNE1 mRNA in m6A‐dependent manner, representing a promising therapeutic strategy for the treatment of CRC. The gene discussed is CCNE1; the disease is colorectal carcinoma.