However, deficiency in signalling via type I interferon receptor (IFNAR1) led to increased activation of lung ILC2, susceptibility to i.n. infection with H1N1 influenza A virus /Puerto Rico/8/1934 (PR8) and infection‐associated type 2 immunopathology in mice in comparison to wild‐type C57BL/6 counterparts.29, 30. The gene discussed is IFNAR1; the disease is infection.