As described in the literature, treatment of CML cells by TKI up-regulates CXCR4, thus promoting cell migration back to bone marrow stroma [8,49], and therefore results in BCR-ABL inhibition, decreased tyrosine phosphorylation, and restored PKA activation [50]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.