More than 95% of patients harbor a characteristic reciprocal chromosomal translocation product, called BCR-ABL1, that originates in a HSC and leads to overexpression of its protein (p210BCR-ABL), with constitutively activated tyrosine kinase activity, giving rise to and sustaining the CML clone [55,56,57]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.