We reported here an RUNX1-Evi-1 transgenic zebrafish model with a phenotype that recapitulated main aspects of human AML such as distorted proliferation, anti-apoptosis, anemia, increased immature myeloid cells and their precursors accumulated in peripheral circulation and kidney marrow (kidney marrow serves throughout the life of a zebrafish, generating adult hematopoietic cells, just like human’s bone marrow [20]), which suggested that RUNX1-Evi-1 played a role in the etiology of AML. This evidence concerns the gene RUNX1 and anemia (phenotype).