These results could support previous findings showing that viral infections can hamper the intrinsic cellular STING and other anti-viral responses, thereby leading to innate immune evasion (Deschamps and Kalamvoki, 2017; Drayman et al, 2019; Hare et al, 2020; Sun et al, 2015), and highlights that microenvironmental spread of cGAMP and/or released dsDNA to the neighbouring cells can be a source of STING activation in an infected cell population. The gene discussed is STING1; the disease is viral infectious disease.