Recent studies have revealed that the human ABCG2 transporter is a P-glycoprotein that causes multidrug resistance (MDR) including mitoxantrone, doxorubicin, and topoisomerase I inhibitors of irinotecan, topotecan, and 7-ethyl-10-hydroxycamptothecin (topoisomerase inhibitor) and gefitinib (an inhibitor of EGF receptor) in patients with lung cancer [41, 43] . Hirschmann-Jax and colleagues were the first to observe that ''side population'' cancer stem-like cells isolated from cell lines and patients with neuroblastoma expressed high levels of ABCG2 and ABCG3 transporter genes as well as a greater capacity to expel cytotoxic drugs [44] . Monzani and colleagues further showed that cancer stem-like cells derived from the melanoma cell line highly coexpressed CD133 and ABCG2 markers with enhanced tumorigenic potential [45] . In this study, we found that LC-CD133 + are highly co-expressed with ABCG2 transporter and are significantly resistant to conventional treatment methods compared with LC-CD133 2 (Figs. 2 & 4) . Interestingly, a significant down-regulating of ABCG2 expression and an increase in the chemosensitivity of LC-CD133 + were observed when the Oct-4 siRNA treatment was given (Data not shown). Thus, more studies are needed to investigate whether over-expression of Oct-4, CD133, and/or ABCG2 play a role in the development of MDR in LC-CD133 + or surrogate markers of therapeutic response in patients with lung cancer.