Oncogenic alterations in ABLs, including fusion protein formation caused by chromosome translocations in leukemia [e.g., BCR-ABL1 in Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia (CML)] and amplification and somatic mutations in solid tumors, constitutively activate ABL-mediated signaling pathways and promote survival, proliferation, dedifferentiation, migration, and invasion in cancer cells135. The gene discussed is ABL1; the disease is cancer.