Additionally, our data suggests indirect mechanisms by which METTL3 modulates AS in breast cancer through m6A deposition on splicing factors and transcriptional regulators of splicing factors such as MYC. Notably, our analyses reveal that m6A deposition correlates with intronic regions and depletion of METTL3 results in more exon inclusion for specific genes. The gene discussed is METTL3; the disease is breast carcinoma.