To investigate this putative contribution of Kat2a loss to preleukemia progression, we crossed conditional Idh1R132H and Kat2aFlox/Flox mice, into the Mx1-Cre background (Fig. 1A), to generate Idh1R132H animals that were heterozygous (HET) or NULL for Kat2a (fig. This evidence concerns the gene MX1 and myelodysplastic syndrome.