We next tested the impact of Kat2a loss on the preleukemia model driven by the exon 9a splicing variant of the RUNX1-RUNX1T1[RT1(9a)] fusion gene (17), which, when retrovirally delivered to adult BM cells, leads to long-latency, incomplete-penetrance leukemia in irradiated recipients (19–20). This evidence concerns the gene RUNX1 and myelodysplastic syndrome.