In this chapter, we describe model systems to study leukemia driven by the Abelson oncogene. In people, the Abelson oncogene results from the chromosomal translocation t(9;22)(q34;q11) that is found in more than 90 % of all human chronic myeloid leukemia (CML) patients and in 20-25 % of patients suffering from acute lymphoid leukemia (ALL). This translocation is also called Philadelphia chromosome and encodes the BCR/ABL oncogene, a constitutive active tyrosine kinase. BCR/ABL renders hematopoietic cells independent from exogenous growth-stimulatory signals by continuously engaging signaling pathways including JAK-STAT signaling and the MAPK pathway. The enforced expression of BCR/ABL suffices to transform hematopoietic cells which made it to one of the best studied model systems in the field. Here we present methods to study BCR/ABL-triggered leukemia and solid lymphoid tumor formation.