SF3B1 and cancer: For instance, oncogenic mutations in spliceosome components SF3B1 and U2AF1 result in the aberrant use of alternative branchsites (Alsafadi et al., 2016; Ilagan et al., 2015; Shiozawa et al., 2018), and cryptic splice sites (Darman et al., 2015; Kesarwani et al., 2017) that often disrupt splicing of cancer‐associated transcripts (Ilagan et al., 2015; Kesarwani et al., 2017).