These findings suggest a complex interplay between sulfatide-induced acetylation, the Mettl3–Mettl14–WTAP complex, m6A methylation, and the transcription factor MTF1, highlighting their potential significance in HCC pathogenesis and progression.[56] It was also found that Mettl3 positively regulates abnormal spindle-like microcephaly (ASPM) through m6A modification, whereas overexpression of ASPM promotes the growth and metastasis of hepatoma cells. The gene discussed is MTF1; the disease is hepatocellular carcinoma.