IFN-γ was shown to play a pathogenic role in MA-ARDS development, as the infection of IFN-γ signaling-deficient mouse models were protected from lung injury despite the increased transmigration and infiltration of leukocytes and activated effector T cells in the lung tissue (Belnoue et al., 2008; Villegas-Mendez et al., 2011; Claser et al., 2019; Galvao-Filho et al., 2019) (Table 2). Here, IFNG is linked to microtia.