A redundant and complex network of cytokines and chemokines directs the pathogenesis of sarcoidosis: in the early phases, the sites of active disease are characterized by an overproduction of Th1/Th17 cytokines, such as interleukin (IL)-2, IFN-gamma [5], and IL-17 [1], associated with the high expression of macrophage-derived molecules like IL-15 [5], CXCL16 [6], CXCL10 [7], CCL20 [8], and CCL5 [9]. The gene discussed is IFNG; the disease is sarcoidosis.