Table 1 describes the phenotype of the resulting Cux1low;NrasG12D mice, which mimic an AML-like disease compared to Cux1mid;NrasG12D mice which are more MDS/MPN similar to that of JMML/CMML, indicating that the further decrease of Cux1 expression drives a more penetrating phenotype in cooperation with NrasG12D to drive AML [39]. The gene discussed is CUX1; the disease is myelodysplastic syndrome.