The pulmonary microenvironment of patients with sarcoidosis is characterized by a well-known highly polarized Th1/Th17 profile [1, 6], where cytokines such as IFN-γ, TNF-α, IL-2, IL-12, IL-17, IL-18, together with several chemokines, induce and maintain an inflammatory state further exacerbated by the constant recruitment of immune cells into the lung. The gene discussed is IL17A; the disease is sarcoidosis.