It thus remains possible that the redundant immunosuppressive activities of the other potent toxins produced by B. pertussis, such as the adenylate cyclase (CyaA) or pertussis (PT) toxins, may have masked the contribution of the increased activity of Bp BteAΔA503 to immune evasion and persistence of the bteAΔA503 mutant in infected lungs. The gene discussed is F2; the disease is pertussis.