When NF- κВ activity is diminished through deletion of IKK-2, it is shown in mouse macrophages that STAT1 activity is enhanced [15].This enhanced STAT1 activity contributes in M1 macrophages to the production of nitric-oxide (NO) through inducible NO synthase (iNOS) and the secretion of pro-inflammatory chemokines and cytokines, such as interleukin (IL)-1β, IL-6, IL-12, IL-23 and TNFα, that attract other components of the pro-inflammatory response to eliminate infections [4,16]. The gene discussed is STAT1; the disease is infection.