Rescue experiments showed that overexpression of METTL3 reversed the inhibition of CRC cell proliferation caused by butyrate, indicating the important role of metabolites in m6A modification.[42] Previous studies reported that butyrate can act as a histone deacetylase inhibitor to epigenetically regulate gene expression.[97] Therefore, we speculated that the butyrate may regulate METTL3 expression and m6A modification in a histone deacetylase manner. This evidence concerns the gene METTL3 and colorectal carcinoma.