Interestingly, both METTL3 and METTL16 have been found to participate in translation independently of m6A-modification, contributing to tumorigenesis [98, 105], despite their primary roles as m6A writers and their predominant action via m6A. Given the increasing evidence emphasizing the significance of translation control by METTL3 and METTL16, especially in cancer contexts, developing drugs that selectively target their translation-related activity while preserving their methylation function could offer a promising therapeutic avenue. This evidence concerns the gene METTL3 and cancer.