In contrast to clinically approved oncogene-targeted therapies for various other malignancies, e.g., imatinib for BCR/ABL-positive chronic myeloid leukemia (CML) or EGFR and ALK inhibitors for EGFR-mutant and EML4/ALK-rearranged NSCLC, respectively [11,12,13,14], the development of a “magic bullet” against mutant KRAS has remarkably challenged scientists and physicians alike because it had long been considered “undruggable” due to biochemistry constraints [15]. Here, ALK is linked to chronic myelogenous leukemia, BCR-ABL1 positive.