Contrary to proliferating leukemic cells, LSCs have been shown to be “BCR-ABL oncogene independent” as demonstrated by their capacity to maintain and reinitiate the disease even after BCR-ABL activity has been shut down in the SCLtTA/BCR-ABL double transgenic CML mouse model [71]. Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.