This observation, together with the Th17/neutrophilia phenotype observed in M. tuberculosis-infected B cell-deficient mice (Figures 1–3), led us to hypothesize that B cells and humoral immunity, by virtue of their ability to modulate the IL-17 response and neutrophilia (Figures 1–3) upon exposure to mycobacteria, may affect the efficacy of anti-TB vaccine. The gene discussed is IL17A; the disease is tuberculosis.