We therefore asked whether repression of MS4A3 could play a role in EVI1-mediated drug resistance of human myeloid leukemic cells [20,27,70], yet re-expression of MS4A3 in U937_EVI1 cells did not re-sensitize them to drugs used in the treatment of AML (JE and SK, unpublished results). This evidence concerns the gene RUNX1 and acute myeloid leukemia.