METTL3 and cancer: After METTL3 knockout, the distribution of the translation initiation factor eIF3 core subunit eIF3b, the cytosolic m7G cap-binding protein eIF4e, and the nuclear m7G cap-binding protein CBP80 shift from heavier multimeric components to lighter submultimeric fractions, resulting in attenuated translation and inhibiting cancer cell survival, growth, and invasion [123].