We expected one of three outcomes: consistently elevated IFNβ responses across the mutant pneumococci, matching the observations with NF-κB activity (Figure 1); a ramping up of IFNβ responses with peak levels after infection by the double mutant Δpde1Δpde2 strain, based on how c-di-AMP content in pneumococci increase due to phosphodiesterase mutations (26); or no effect of phosphodiesterase mutation, based on the postulate that pneumococcal DNA but not c-di-AMP drives IFNβ responses (19). The gene discussed is NFKB1; the disease is infection.