These results above indicate that in response to drug treatment, increased Cer glycosylation transactivates the expression of METTL3 by the cSrc and β‐catenin signaling pathway and the resultant m6A at the mutant‐codon lends to preferential pre‐mRNA splicing so as to amplify mutant protein production in cancer cells carrying TP53 R373H mutation. This evidence concerns the gene METTL3 and cancer.