The bacteria bind to and invade M cells within the follicle-associated epithelium overlying the lymphoid follicles of the Peyer��s patches. Following their entry into PPs, the bacteria induce the host immune response, which is characterized by an inflammation with infiltration of neutrophils and macrophages. Nod2 has been identified as an intracellular receptor of the innate immune system. It is involved in the recognition of pathogen associated molecular patterns present in the bacterial cell wall but little is known about its role during the host response towards pathogenic bacteria. We show that Nod2 is involved in the in vivo response towards Y. MK-4827 pseudotuberculosis. This phenotype is not dramatic, as indicated by the limited differences observed in the LD50 between knock out and wild-type mice. However, this result is meaningful as indicated by its reproducibility in several mouse models and in several genetic backgrounds. Interestingly, the same phenotype is observed in a knock out model and in a model of mice carrying a mutation homologous to the main Human CD associated mutation. This mutation is usually considered as a loss of function mutation in Human while it has been associated with an over stimulation of the IL-1b pathway in mouse. It is out of the scope of this paper to fully resolve the question but it is to note that our results suggest that it is possible to conciliate the two models at least in terms of the immune response to Y. pseudotuberculosis. In addition to the above expression studies, recent molecular and biochemical studies have alluded to the role of AQPs in human carcinogenesis. AQP1 is shown to play a role both in angiogenesis and cell cycle control, assisting cancer development. Our group has reported that the expression of wildtype AQP5 in a NIH3T3 mouse fibroblast cell line induced many phenotypic changes characteristic of transformation in vitro and in vivo by triggering signaling pathways activated through Ras, which is induced by phosphorylation of the PKA consensus site of AQP5. Interestingly, Talazoparib athymic mice injected with NIH3T3 cells stably transfected with AQP5 exhibited a robust tumor formation. Most recently, we have demonstrated that AQP5 promotes cell proliferation and that its overexpression is related with liver metastasis; we have also found molecular pathways based on the Ras/ERK/Rb signaling pathway as a mechanism to promote cell proliferation in colon cancer cells. Previous expression studies of AQP5 in human tissues, both normal and malignant, have been only in epithelial tissues and carcinomas. For instance, lung epithelium is a well known site of AQP5 expression and the expression level of AQP5 seems to be higher in non small cell lung cancer than in normal lung tissue. Of interest, it has been reported that aspirates of bone marrow cells, fresh or cultured, can express AQP5, typically expressed in the type I pneumocyte, and that bone morrow derived cells can be precursors of differentiated parenchymal cells of the lung.