RUNX1 and myelodysplastic syndrome: Mice with compound mutations of Tet2 and N-ras (Mx1CreTet2fx/fxN-rasG12D) developed accelerated CMML or AML [143, 144]. In addition, cooperation of Tet2MT with Ezh2, Asxl1, or Bcor mutations in MDS/MPN, Tet2MT with Jak2V617F in MPN, Tet2MT with Flt3ITD, Aml1-Eto, Pu.1UREΔ/WT, or Ncstn mutations in AML, and Tet2MT with KitD816V in mastocytosis have been also evaluated in mouse models (Table 2).