Puzzled by the striking discrepancy between exaggerated phagocyte accumulation in the spleen and liver of Lm-infected ADAPko mice (Figure 2) versus the strongly delayed pathogen elimination (Figure 1B), we next investigated whether infection-associated activation of phagocytes in an ADAP-deficient host would affect the production of the pro-inflammatory mediators TNF-α, IL-1α, and iNOS by these cells. This evidence concerns the gene IL1A and infection.