Notably, pathological features of neuroinflammation, neuropathology, and motor defects in human Niemann–Pick disease type C reconstructing in Npc1−/− mice are significantly improved by genetic deletion of Sting or Irf3, but not deletion of Cgas, which indicates the predominant function of ligand-independent STING activation in disease progression and that pharmacological inhibition of STING activation maybe a promising strategy for the treatment of Niemann–Pick disease type C (Chu et al., 2021b). The gene discussed is CGAS; the disease is Niemann-Pick disease type C.