Acquired resistance to imatinib in chronic myeloid leukemia (CML) and gastrointestinal stromal tumor (GISTs) through a secondary gene mutation in BCR-ABL and KIT genes, respectively, are examples of the adaptive capability of cancer cells to kinase inhibitors [178, 179]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.