Marais and colleagues demonstrated that some ABL1/2 and DDR1 inhibitors weakly bind RAF (following 3 h treatment), and induce RAF heterodimerization and paradoxical MEK/ERK activation in chronic myelogenous leukemia cells harboring a drug-resistant form of BCR-ABL (T315I) and tumor cells with activated RAS [55]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.