A monomer-hexamer equilibrium, similar to that observed for MtbRho, has also been seen for Mtb Mfd protein although the trigger that causes a shift towards monomer or hexamer was not yet identified. The monomeric form of Mtb Mfd protein is considered to be the functional one, while the hexamer is likely to be a ‘storage state’. In case of MtbRho, it appears that nascent RNA could be driving the oligomerization of the termination factor to its functional form. Triple-negative breast cancer is a subtype of breast cancer, defined by the lack of estrogen receptors, progesterone receptors and human epidermal growth factor receptor 2. The triple-negative subtype accounts for 12% to 24% of human breast cancers and is associated with a significantly higher rate of relapse and lower overall survival rate than other breast cancer Reversine subtypes. Despite the high sensitivity of triple-negative breast cancer to initial chemotherapy, the high rate of early recurrence and the absence of targeted therapies have been major challenges to treat these patients. Approximately 20% of triple-negative breast patients carry BRCA mutations; thus drugs affecting the DNA repair system, such as platinum compounds and poly ADP ribose polymerase inhibitors, have been investigated as potential therapies. However, the other 80% of triple-negative breast cancer patients without BRCA mutations might not benefit from those therapies, requiring the development of new therapeutic agents. Cancer stem cells are the subpopulation of cancer cells shown to be required for sustained tumor growth and progression as well as for tumor recurrence and metastasis. Interestingly, many of the signaling pathways that regulate normal stem cells, such as Wnt, Hedgehog and Notch, are aberrantly activated in cancer stem cells. Since the activation of stem cell signaling pathways is required for the maintenance of these cells, new experimental agents inhibiting these pathways are being developed to target cancer stem cells. CDDO, 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid, is a synthetic triterpenoid derived from the naturally occurring triterpene oleanolic acid. To further increase its anticancer and anti-inflammatory properties, numerous derivatives of CDDO, such as CDDO-methyl ester, CDDO-ethyl amide and CDDO-imidazolide, were developed. CDDO-Im is one of the most potent synthetic triterpenoids shown to induce growth inhibition and apoptosis in various human cancer cells, including multiple myeloma, lung, pancreas and breast cancer. In breast cancer, CDDO-Im is effective on both ER-positive and ER-negative breast cancer cells. Development of mammary tumors in the HER2-overexpressing animal model was delayed by CDDOIm. A recent study also demonstrated that CDDO-Im induced apoptosis in BRCA1-deficient breast cancer cells by increasing DNA damage and G2/M arrest. In the present study, we investigated the effect of CDDO-Im on the cancer stem cell subpopulation in triple-negative breast cancer cells.