These observations lend support to the complexity of the pathways affected by these inhibitors as also indicated by the less than desired results obtained by combining inhibitors of Bcr-Abl and mTOR in the clinical management of both CML and gastrointestinal stromal tumors that harbor activating mutations in receptor tyrosine kinases [29], [31]. The gene discussed is NTRK1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.