METTL3 and hepatocellular carcinoma: Therefore, we propose a novel inactivation mechanism of HCC oncogenes using two steps of posttranscriptional regulation, alternative splicing and RNA modification, in which the alternatively spliced variant of METTL3 antagonizes the function of its canonical full-length isoform, decreasing the m6A modification and thereafter altering the mRNA decay/stability of HCC oncogenes.