IFNG and sarcoidosis: Mechanisms underlying the transition from inflammatory to fibrotic disease in the lung of sarcoidosis patients are not entirely elucidated, but this complex process is at least in part sustained by increased production of fibrosis-stimulating cytokines (such as TNF-a, IFN-g, TGF-b, IL-10, IL-13) in the granuloma microenvironment [47].