Given that EGFR is a downstream target of METTL3, Wang et al. discovered that METTL3 was identified as the most notably increased protein among these m6A regulators in HCC cells that are resistant to lenvatinib, and inhibition of METTL3 increased cell apoptosis upon lenvatinib treatment, which overrode LR 40. Here, METTL3 is linked to hepatocellular carcinoma.