However, IL-17A deficiency in mice significantly reduced the occurrence of both fibrosis and pneumonitis after exposure to radiation, confirming that IL-17A is deeply involved in the development of RIPI.14 Wang et al.68 provided more evidence to support the importance of IL-17A in the development of RIPI and showed that blocking IL-17A signaling by IL-17A-neutralizing antibodies significantly reduced the occurrence (percentage) of severe alveolitis (grades II and III) induced by single-dose irradiation of the thorax in mice. The gene discussed is IL17A; the disease is pneumonitis.