Deletion of c-Abl results in defects in embryonic hematopoiesis resembling those seen here33,34, and constitutive activation of c-Abl via the t(9;22) increases HSC survival and proliferation and generates chronic myeloid leukemia (CML)35–37. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.