METTL3 is highly expressed in HCC and is closely associated with poor prognosis of HCC patients, and promotes HCC cell proliferation, migration, metastasis and tumorgenicity via YTHDF2-dependent post-transcriptional silencing of SOCS2, which is a member of the suppressor of cytokine signaling (SOCS) family, and is a negative regulator of the JAK/STAT pathway (Chen et al., 2018). The gene discussed is CISH; the disease is hepatocellular carcinoma.