The previously identified U2AF1 p.S34F mutation (Figure 2A), located in the same ZnF in myelodysplastic syndrome (MDS) patients, was shown to disrupt splicing of a number of cancer-relevant genes leading to overall dysregulation of several downstream pathways including epigenetic regulation and DNA damage response [29, 30–32]. Here, U2AF1 is linked to myelodysplastic syndrome.