The results of the present study demonstrated that METTL14 was transcriptionally activated by wild‐type p53 and positively modulated the processing of pri‐miR‐6769b/pri‐miR‐499a in an m6A‐YTHDF2‐dependent manner, which selectively enhanced the maturation of miR‐6769b‐3p/miR‐499a‐3p and down‐regulated SLC2A3/PGAM1, respectively, thus attenuating glycolysis and tumor development in p53‐WT CRC. Here, YTHDF2 is linked to neoplasm.