A study conducted almost recently uncovered that nuclear AURKA exerts a pivotal effect on lung cancer tumorigenesis by mediating the interaction between the m6A reader YTHDC1 and the splicing factor SRSF3 or hnRNPK to regulate the alternative splicing of RBM4, revealing how a reader of m6A modification acts as a switch for an oncogenic splicing event triggered by a tumorigenic signal in lung cancer. The gene discussed is AURKA; the disease is lung cancer.