Interestingly, a recent study describing a murine model of U2AF1-S34F, another MDS-associated splicing gene mutation associated with aberrant 3′ splice acceptor site recognition, also showed limited mouse–human overlap of mispliced transcripts.33 The mouse–human overlap appeared greater for a mouse model of SRSF2 mutations (SRSF2-P95H), another commonly mutated gene in human MDS, possibly because the splicing aberration involves alternative exonic sequences, which are more likely than intronic ones to be conserved.34 Here, SRSF2 is linked to myelodysplastic syndrome.