MYC and breast carcinoma: 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.