The lung fibrosis process is the final result of a complex homeostatic alteration involving inflammation, oxidative stress, chemoattractant mediators, and coagulation abnormalities, with cytokines such as TGF-β1, PDGF, IL6, IL11, and IL17 driving the underlying pro-inflammatory and profibrotic mechanisms [1]. The gene discussed is IL17A; the disease is pulmonary fibrosis.