U2AF2 and cancer: To further explore this relationship, we examined RNA-seq data from Fubp1- knockout mice and a CRISPR-engineered RPE1 cell line carrying the cancer-associated A38D point mutation, disrupting FUBP1’s interaction with the splicing factor U2AF2 and impairs efficient splicing of long introns.40 In both models, Thbs2 expression was significantly reduced, consistent with a broader role for FUBP1 in regulating Thbs2 expression (Fig. S5E).