Because a compensatory role and context-dependent interaction between Gsdmd and Ripk3 have been described24,25, we generated Gsdmd−/−Ripk3−/− SKG mice by crossing Gsdmd−/− SKG and Ripk3−/− SKG mice to assess whether Ripk3 or Gsdmd could compensate for a Gsdmd- or Ripk3-deficient condition, respectively, in the development of autoimmune arthritis, and evaluated their arthritis phenotypes and the development of Th17 cells in Gsdmd and Ripk3 double-deficient conditions. This evidence concerns the gene RIPK3 and Arthritis.