Compared with untreated CML patients, the lymph node mononuclear cells of imatinib-treated CML patients showed AP-1 activation, as well as downregulation of pro-inflammatory cytokines (88), which could be caused by the inactivation of JunB gene methylation, indicating that JunB could be a tumor suppressor gene (89). Here, JUN is linked to chronic myelogenous leukemia, BCR-ABL1 positive.