Taken together, these data suggest that the increased liver burden in IKKβ cKO mice or granuloma maintenance were due to defects in myeloid function related to control of bacterial growth and spread of infection rather than overt initial increases in macrophage infection (Fig. 5B) or loss of cells from the myeloid compartment (Fig. 6A–B). The gene discussed is IKBKB; the disease is Granuloma.