It was designed to inhibit the fusion gene resulting from a chromosomal translocation (BCR-ABL) tyrosine kinase fusion protein in chronic myeloid leukemia (CML) and imatinib established the paradigm of structure-based drug design and opened the door for an entire class of kinase inhibitors.9,10 Since then, medicinal chemists have engineered inhibitors targeting epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), B-Raf proto-oncogene, serine/threonine kinase (BRAF), and other kinases with unique selectivity and clinical impact.11 This evidence concerns the gene BRAF and chronic myelogenous leukemia, BCR-ABL1 positive.