Upregulation of CD44, along with increased binding to E-selectin, is observed in BCR-ABL-expressing cells with the T315I mutation, and these cells, which adhere to stromal cells, are quiescent [37], suggesting that these alterations of extrinsic factors by CML LSCs promote exclusive LSC lodging and dormancy, allowing them to escape TKI targeting. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.