Imatinib, a BCR-ABL tyrosine kinase inhibitor, is capable of inducing major or complete cytogenetic responses in most CML patients [23, 24], changing dramatically the 10-year overall survival from 20 to 80–90% [7, 25]; however, it has been documented that it penetrates poorly into the CSF [6, 11, 26], probably due to increased efflux of the drug from the CNS due to P-glycoprotein [27]. This evidence concerns the gene ABCB1 and chronic myelogenous leukemia, BCR-ABL1 positive.