Surprisingly, while pathologic examination of moribund Cux1+/−Flt3ITD mice culled at an earlier age revealed infiltration of liver, spleen and bone marrow with excessive numbers of myelomonocytic cells leading to effacement of normal tissue architecture compatible with a diagnosis of CMML (Fig. 2h–k; square symbols Fig. 2a), older animals succumbed to AML following on from prior CMML (circle symbols Fig. 2a). Here, CUX1 is linked to chronic myelomonocytic leukemia.