The concept of disparate activity of the IFN-γ-induced CXC chemokines in the context of Th1-like immune disorders, such as sarcoidosis, was originally raised by Agostini et al. [69] who documented an enhanced expression of IP-10 in sarcoid tissues and a positive relationship of BALF IP-10 levels and the degree of T-cell alveolitis, suggesting its pivotal role in ruling the migration of T-cells to sites of ongoing inflammation. The gene discussed is CXCL10; the disease is sarcoidosis.