In AML patients, mutations and CNVs of m6A regulators are associated with the presence of TP53 mutations.18 Now that epigenetic modifications are unlikely to induce genomic alterations, we inferred that changes of m6A regulators as well as corresponding molecular/phenotypical events in GC were elicited by upstream mutations, probably through activation of cancer driver genes or loss of tumor suppressor genes. The gene discussed is TP53; the disease is neoplasm.