For example, G2/I2 showed hyper-editing of type 1 interferon (IFN) receptors (IFNAR1 and IFNAR2), type 1 IFN-stimulated genes (ISGs) (e.g., EIF2AK2, DDX58/RIG-1, MAVS, TRIM56, and TRIM69) and genes involved in immune responses to viral infection (EIF2AK2, DDX58/RIG-1, MAVS, CASP8, CYCS, and HMGB1) [57,58] (Figure 4c). The gene discussed is IFNAR2; the disease is viral infectious disease.