Studies in mice have demonstrated that natural infection with B. pertussis induces antigen-specific interleukin 17 (IL-17)– and/or interferon-γ (IFN-γ)–secreting CD4 TRM that persist in the lung and nasal cavity, and subsequently proliferate locally and mediate rapid clearance of bacteria following reinfection [4, 8, 9]. The gene discussed is IFNG; the disease is infection.