Translation of biomarkers from mouse to man however should be performed with care. Overall, our study describes the molecular and cellular sequence of events that eventually lead to the induction of protective immunity to pertussis, including local immunity in the lungs, which is not induced by current vaccines. Especially the inductions of Th1 and Th17 cells and IgA in the lungs are regarded key elements in superior immunity. Our data can be used to select vaccine concepts that resemble infection, with respect to e.g. administration route and prolonged antigen exposure, and immune signatures elicited. Local delivery of vaccines may be an important advancement for improved protection as was previously demonstrated with a live attenuated pertussis vaccine. Also adjuvants could be selected and optimized that can steer host immunity of inactivated vaccines towards an infection-like immune response with minimal adverse effects. The molecular and cellular fingerprint of the local immune response discovered in B. pertussis Ginsenoside-F4 infected mice thus can provide a strong guidance for developing improved pertussis vaccines. KLF4 has been shown to regulate cell proliferation and differentiation, its role has been extensively investigated in several human cancers by using gain- and loss-of-function approaches. In colon and prostate cancer, KLF4 acts as an oncogene. In contrast, it plays a tumor suppressor role in neuroblastoma, lung cancer, gastric cancer, lymphoma, cervical cancer, pancreatic ductal cancer, and Dimesna hepatocellular carcinoma. In breast cancer, KLF4 can function both as an oncogene and a tumor suppressor. The role of KLF4 in ovarian cancer has not been adequately and mechanistically addressed. A previous study indicates that the expression level of KLF4 was significantly reduced in ovarian cancer compared to normal ovarian epithelium, suggesting that KLF4 might potentially act as a tumor suppressor in ovarian cancer. KLF4 plays a unique role in stem cell reprogramming by facilitating the mesenchymal to epithelial transition. The cellular phenotypic switch from epithelial to mesenchymal cell transition is a fundamental process in tumor metastasis that is a prominent feature of ovarian carcinomas. The MET or EMT leads to the alterations of epithelial and mesenchymal marker gene expression that include snail1 & 2, Zeb 1 &2, Twist, vimentin, Ecadherin. EMT is regulated by multiple signaling pathways, which include WNT, TGFb, and Notch.. Recent studies indicate that miRNAs regulate EMT or MET pathways by targeting epithelial or mesenchymal cell marker genes that include miR-194, miR-203, and miR-200c. KLF4 has been shown to regulate EMT in several different cancer cells. In hepatocellular carcinoma, breast, and prostate cancer cells, KLF4 activates the transcription of the epithelial cell marker gene Ecadherin and represses the mesenchymal cell marker gene snail 2 by binding to their respective promoters. KLF4 in these cancers promotes MET and inhibits tumor cell growth. In the present study, we investigated the role of KLF4 in ovarian cancer cells using a doxycycline -dependent KLF4-inducible lentiviral vector and found that inducible overexpression of KLF4 reduced cell proliferation, migration, and invasion through promoting MET in ovarian cancer cells. In this study, we investigated the role of KLF4 in ovarian cancer cells using lentiviral vector mediated inducible expression.