These results have led to increased off-label use of molecularly targeted agents on the basis of identified molecular alterations, such as BRAF V600 mutations for administration of anti-RAF and anti-MEK therapies in melanoma [8], BCR-ABL gene fusions for the use of imatinib in treating chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) [9], and the loss of PTEN expression for administration of resistance to anti-EGFR monoclonal therapy [10]. This evidence concerns the gene MAP2K7 and chronic myelogenous leukemia, BCR-ABL1 positive.