The tyrosine kinase inhibitor, imatinib, was found to mediate gene expression changes of SP1 (upregulation) and DNMT1 (downregulation) resulting in demethylation of the CD70 promotor in CML cells and thus upregulated CD70 expression and compensatory Wnt signaling in CML cells [45]. The gene discussed is SP1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.