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For instance, through DNMT3B, methylglyoxal (MG), a byproduct of glycolysis, can cause hypermethylation of tumor suppressor genes in breast cancer [55], demonstrating that metabolites act as “epigenetic messengers.” It is unclear, nevertheless, whether MG controls DNMTs in TC (especially the BRAF V600E mutant subtype) via a comparable mechanism, causing essential tumor suppressor genes, such as RASSF1A or PTEN, to become hypermethylated and promoting dedifferentiation and treatment resistance