However, comparison of infected AM to uninfected AM from mice three to six weeks after infection, shows that Mtb-infected AM are highly activated, upregulated IFNγ-regulated genes (e.g., NOS2, H-2, CD274 and CD38), upregulated IL-1 and COX-2, and downregulate Alox5 and PPARγ, compared to uninfected AM, all of which should foster an environment that restricts bacillary growth [34, 39–41]. The gene discussed is PTGS2; the disease is infection.