On the one hand, metabolic reprogramming influences the methylation status of tumor suppressor genes and thyroid function genes by dynamically regulating the activity of DNA methyltransferases and demethylases through important metabolites (such as S-adenosylmethionine, or SAM, and α-KG) and oncogenic signaling pathways (like PI3K/AKT). This evidence concerns the gene AKT1 and neoplasm.