There has also been some evidence that deposition of dsDNA in joints might be responsible for the inflammation observed in rheumatoid arthritis patients [18], although it is unlikely that cGAS/STING inhibitors will be superior to the TNF blockers that are used in the clinics: evidence from preclinical models suggests that TNF also controls, among others, the cGAS activation in joint inflammation [19]. This evidence concerns the gene CGAS and rheumatoid arthritis.