Chromosomal rearrangements involving ABL1 occur in various hematological malignancies leading to fusions of the ABL1 gene to different fusion partners. The translocation t(9;22)(q34.1;q11.2) results in BCR/ABL1 fusion and is observed in approx. 90% of patients with chronic myeloid leukemia (CML) and in approx. 25% of adults with acute lymphoblastic leukemia (ALL). The rearrangements are cytogenetically characterized by the presence of the Philadelphia (Ph) chromosome. Other ABL1 fusion partners include, e.g., ETV6 and NUP214. The kinase domain of ABL1 is retained in all chimeric proteins. The NUP214-ABL1 is the second most prevalent ABL1 fusion gene in malignant hemopathies, with a frequency of 5% in T-cell ALL. NUP214-ABL1 fusion genes are often found amplified on episomes. Tyrosine kinase inhibitors, such as imatinib, suppress the constitutive kinase activity of ABL1 fusion proteins. Therefore, these drugs may have potential in the treatment of patients with ABL1 fusions.