Our results showed that the turnover of DSN1 mRNA was markedly accelerated in SRSF9-inhibited cell lines (Fig. 6L), while the half-life of DSN1 mRNA was markedly prolonged in SRSF9-overexpressing cell lines (Fig. 6N) and such stabilizing was weakened upon m6A writer knockdown (Fig. 6P), indicating that SRSF9 promotes the stability of DSN1 mRNA and such regulation is correlated with its RNA m6A modification in CRC cells. Here, SRSF9 is linked to colorectal carcinoma.