In human SF3B1-mutant MDS, ring sideroblasts are thought to arise as a result of aberrant splicing of key genes involved in heme biosynthesis, such as ABCB7, TMEM14C, ALAS2 and SLC25A37. 11, 25, 30, 35 In keeping with the mouse–human differences in target transcripts, we did not find the splicing or expression levels of any of these genes to be noticeably disrupted by Sf3b1-K700E, and, consistent with this, did not identify ring sideroblasts in the bone marrow of mutant mice. The gene discussed is TMEM14C; the disease is myelodysplastic syndrome.