This study showed that by eliciting K+ efflux from dendritic cells, and perhaps some other CD11b-expressing phagocytes, the pore-forming activity of CyaA contributes to activation of the NALP3 inflammasome and thereby to induction of innate IL-1β response, which supports the clearance of Bordetella bacteria at later stages of infection. The gene discussed is ITGAM; the disease is infection.