For instance, METTL3 and METTL14 were shown to be oncogenic in AML24–26 but tumor suppressive in GBM.16 Curiously, even for the same cancer type (e.g., GBM), the role of the same gene (e.g., METTL3) was reported to be discordant in independent studies.16,27 These studies highlight the imperative need for undertaking systematic, large-scale studies in independent patient cohorts to unravel the true clinical potential of m6A regulators in human cancers. This evidence concerns the gene METTL3 and neoplasm.