One possible mechanism by which METTL3 can potentially regulate AS is via the proto-oncogene MYC as: i) it is implicated in AS in breast cancer [56]; ii) MYC mRNA is decorated with the m6A mark which positively regulates MYC expression; and iii) METTL3-mediated DSE significantly overlapped with MYC-regulated DSE, although we cannot disregard the possibility that those AS events are more sensitive to switches upon perturbation of the splicing factor that regulates them. The gene discussed is METTL3; the disease is breast carcinoma.