CSF2 and chronic myelomonocytic leukemia: Studies with an NrasG12D/+ driven mouse model for CMML demonstrated that eliminating GM-CSF signaling via knockout of the GM-CSF beta receptor was insufficient to inhibit leukemia development, but prolonged the survival of mice and reduced splenomegaly of NRasG12D/+ mice, and reduced colony formation of their hematopoietic cells [63].