Interestingly, high SF3B1 levels correlated with higher usage of alternative 3′ splice sites, resembling common alterations in SF3B1-mutated cancers [7], and with elevated exon skipping, which has been linked to PDAC and to SF3B1-mutation in myelodysplastic syndromes [47] and C. elegans models [48]. This evidence concerns the gene SF3B1 and cancer.