The Mettl3-mediated m6A modification of RBM14 via YTHDF1, which supports the M2 phenotypic polarization of Kupffer cells, promotes the growth and metastasis of the tumor.[59] Mettl3 was also found to mediate WW domain-containing protein 2 (WWP2) m6A modification, which was recognized and bound by IWP2BP2, increasing the stability of WWP2 and leading to WWP2 overexpression. The gene discussed is METTL3; the disease is neoplasm.