A recent analysis of the 1918 epidemic, noted that cities where strict interventions were implemented early on to prevent transmission, were overall worse-off than cities where some degree of transmission occurred early on [16] . Given the need for the population to acquire sufficient natural immunity over time, it can not be excluded that the amount of protection conferred by home made masks might sufficiently reduce viral exposure to impact on transmission during the early waves, while allowing people enough exposure to start mounting an efficient immune response. Further field studies are needed to assess acceptability and effectiveness of masks worn by people from the general population. Also, experimental data are needed to develop dose-response models which may improve understanding of determinants of transmission. A cost-effectiveness analysis might give further insights in the relative benefits of home made masks.  Oct-4 Expression Maintained Cancer Stem-Like Properties in Lung Cancer-Derived CD133-Positive Cells CD133 (prominin-1), a 5-transmembrane glycoprotein, has recently been considered to be an important marker that represents the subset population of cancer stem-like cells. Herein we report the isolation of CD133-positive cells (LC-CD133(+)) and CD133-negative cells (LC-CD133(−)) from tissue samples of ten patients with non-small cell lung cancer (LC) and five LC cell lines. LC-CD133(+) displayed higher Oct-4 expressions with the ability to self-renew and may represent a reservoir with proliferative potential for generating lung cancer cells. Furthermore, LC-CD133(+), unlike LC-CD133(−), highly co-expressed the multiple drug-resistant marker ABCG2 and showed significant resistance to chemotherapy agents (i.e., cisplatin, etoposide, doxorubicin, and paclitaxel) and radiotherapy. The treatment of Oct-4 siRNA with lentiviral vector can specifically block the capability of LC-CD133(+) to form spheres and can further facilitate LC-CD133(+) to differentiate into LC-CD133(−). In addition, knock-down of Oct-4 expression in LC-CD133(+) can significantly inhibit the abilities of tumor invasion and colony formation, and increase apoptotic activities of caspase 3 and poly (ADP-ribose) polymerase (PARP). Finally, in vitro and in vivo studies further confirm that the treatment effect of chemoradiotherapy for LC-CD133(+) can be improved by the treatment of Oct-4 siRNA. In conclusion, we demonstrated that Oct-4 expression plays a crucial role in maintaining the self-renewing, cancer stem-like, and chemoradioresistant properties of LC-CD133(+). Future research is warranted regarding the up-regulated expression of Oct-4 in LC-CD133(+) and malignant lung cancer. Lung cancer is one of the leading causes of cancer-related deaths in industrialized countries [1, 2] . Radiotherapy and chemotherapy play significant and crucial roles in clinical antilung cancer treatment to achieve prolonged patient survival [3, 4] . However, a high failure rate and low median survival rate are observed in patients undergoing chemoradiotherapy with recurrent, intractable lung cancer [5] . To improve the patient survival rate, investigation to elucidate the mechanism of tumorigenesis of lung cancer is needed [5] . Recent data have demonstrated that tumors contain a small subpopulation of cells, i.e., cancer stem-like cells (CSCs) or cancer-initiating cells (CICs), which exhibit a selfrenewing capacity and are responsible for tumor maintenance and metastasis [6] . Stem cells have been isolated by their ability to efflux Hoechst 33342 dye and are referred to as the ''side population (SP)'' [7] . Ho and colleagues isolated and characterized SP cells from six human lung cancer cell lines and showed that an elevated expression of ABCG2 as well as other ATP-binding cassette transporters were positively correlated with resistance to multiple chemotherapeutic drugs [8] . In addition, Gutova and colleagues have purified uPAR-positive CSCs from three lung cancer cell lines. These uPAR-positive cells co-expressed with CD44 and MDR1, and had the ability to promote advanced malignancy and chemoresistance [9] .