SF3B1 and cancer: Hotspot mutations in SF3B1 induce use of cryptic 3′ splice sites typically located ∼10–30 nt upstream of the associated canonical 3′ splice sites by promoting recognition of alternative branch sites (Darman et al. 2015; DeBoever et al. 2015; Alsafadi et al. 2016; Zhang et al. 2019a), and some of the resulting splicing errors contribute to severe cancer phenotypes (Inoue et al. 2019; Lieu et al. 2022).