Since interleukin-17 (IL-17) is a major pro-inflammatory cytokine involved in neutrophil recruitment [4], [5] and chronic lung pathologies [6], [7], we hypothesized that IL-1β secreted upon lung injury may induce innate “proTh17” IL-23 and IL-17 expression in lung resulting in pulmonary inflammation and evolution to fibrosis. The gene discussed is IL23A; the disease is fibrosis.