Recently, researchers have uncovered a mechanic link between tumor methionine metabolism and T-cell exhaustion: they showed that SAM and MTA treatment promotes the dysfunction of human CD8+ T cells in vitro, and that knockout of MAT2A reduces SAM production and suppresses tumorigenesis and T-cell dysfunction in hepatocellular carcinoma (HCC) [8]. The gene discussed is CD8A; the disease is neoplasm.