We postulate that wild-type and mutant non-HAd-Ft and even HAd-Ft mutants are severely attenuated not by virtue of an inability to suppress NF-κB-mediated host immunity, but because they aberrantly elicit TNF, IL-1β, IL-6, IL-12, and IFN-γ, immune modulators associated with ‘sterilizing’ innate responses to infection. The gene discussed is NFKB1; the disease is infection.