METTL14 is lowly expressed in HCC, and overexpression of METTL14 is able to promote m6A by increasing the binding of the microprocessor protein DiGeorge syndrome critical region 8 (DGCR8) and pri-miR126 to inhibit HCC progression (Ma et al., 2017). This evidence concerns the gene DGCR8 and hepatocellular carcinoma.