It is well known that cancer associated SF3B1 mutations, which are almost exclusively missense mutations, do not result in the abrogation of SF3B1 expression, but rather change how SF3B1 recognizes 3′ splice sites, often leading to cryptic splice site usage, exon skipping and intron retention, which results in disruption of target gene open reading frames (11, 16). The gene discussed is SF3B1; the disease is cancer.