We speculated that the reason for this might be that a cytosolic DNA sensor, cGAS, competed in order for the substrate ATP to produce more cyclic-GMP-AMP (cGAMP), which binds to and activates the adaptor protein STING, resulting in IRF3 activation and IFNβ induction at the late stage of infection [42]. This evidence concerns the gene IFNB1 and infection.