Alongside the expression of pro-inflammatory cytokine/chemokine and antimicrobial effector molecules, such as NOS2/iNOS, IL-12, and IL-1β, the concurrent induction of immune repressive IL-10 and ARG1 in Mtb-infected macrophages, lungs of mice and rabbits, and in the lung granulomas of active TB patients, suggests a suboptimal macrophage activation (24, 71, 77, 87, 104–106). Here, ARG1 is linked to tuberculosis.