Because infection with intracellular pathogens such as TB necessitates the expression of Th1 cytokines such as IFN-γ, a central macrophage-activating cytokine that is also involved in immune protection against MTB (17), an increase in plasma levels of cortisol and a decrease in DHEA levels may impair the immune response against TB, favoring increased susceptibility and disease progression (18). This evidence concerns the gene IFNG and tuberculosis.