Although there is growing evidence that STING is involved in the generation and maintenance of neuroinflammation and inflammatory bone pain, a recent study in an alternate nerve injury (SNI) model demonstrated that STING activation in DRG neurons drives bone pain through the TBK1/IKK/NF-κB proinflammatory factor signaling pathway; thus, STING may be a new therapeutic FD/MAS pain target for the treatment of FD/MAS pain [61]. This evidence concerns the gene NFKB1 and Fabry disease.