Environmental carcinogens from air pollution and metal exposure have emerged as major sources for inducing cancers. Epidemiological data have shown that hexavalent chromium (Cr [VI]) is linked to cancer development. A list of evidence supports the association between occupational exposure to hexavalent chromium and various cancers, especially lung cancer.1 However, the underlying mechanisms by which Cr (VI) induces cancers are still unclear. As the most prevalent mRNA modification, N6-methyladenosine (m6A) provided a novel form of post-transcriptional gene regulation. m6A regulators were found to be closely correlated with specific malignant tumors, including lung cancer. Among these, METTL3, the core methyltransferase for m6A modification, has gradually attracted much attention due to its cancer-promoting role in multiple cancers.2 However, the exact roles of METTL3 and m6A methylation in carcinogenesis induced by chronic chromium exposure and lung cancer development remain unclear.