The fact that cancer cells exhibited 3′ UTR shortening of HN1 and up-regulation of HNRNPA1 while senescent cells displayed 3′ UTR lengthening of HN1 and down-regulation of HNRNPA1 (Supplementary Figure 10A–10D) can be well explained by the HNRNPA1-mediated APA regulation of HN1. These results prompted us to hypothesize that HNRNPA1-mediated changes in HN1 expression not only can regulate cellular senescence but also have the potential to regulate cancer-associated phenotypes. Here, HNRNPA1 is linked to cancer.