In this experiment, we used BCR-ABL-T315I to induce CML in mice, because we previously showed that compared to wild type BCR-ABL, CML cells harboring BCR-ABL-T315I in mice were more dependant on HSP90 for stability and therefore BCR-ABL-T315I protein was more sensitive to HSP90 inhibition for degradation [9], providing a more sensitive assay for testing the transition of LSCs to LSK- cells. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.