In light of the above, one can assume that if the blockade of NF-κB translocation and of RANKL/RANK interaction does not effectively stop the development of allergic asthma at the level of the clonal expansion of CD4+ Teff cells in the MLNs (i.e., in an inductive site of pulmonary immune response), then it can attenuate it at the pulmonary level (i.e., in an effector site of pulmonary immune response) via the inhibitory effect on IL-4- and IL-17 production by lung infiltrating Th2 and Th17 cells, respectively. The gene discussed is IL4; the disease is allergic asthma.