Recent studies investigated the facets of this complicated interaction, including the suppression of interferon-gamma by interleukin-10 (IL-10) [8], the stimulation of IFN-γ and IL-10 production by IL-12 [9], the stimulation of IFN-γ and IL-10 production by TCD4+ cells in the bronchoalveolar lavage (BAL) fluid of patients with pulmonary TB [10], and the association of Th2 cytokines with histopathologic changes in patients with TB [11]. The gene discussed is IFNG; the disease is tuberculosis.