Furthermore, the lack of interferon γ (IFN- γ) has also been reported to promote the expression of RIPK1, RIPK3 and MLKL in CIA mice, increase the number of Th17 cells, promote the release of IL17 and TNF-α, and activate STAT3, thereby aggravating inflammation and joint damage in RA (176). This evidence concerns the gene IL17A and rheumatoid arthritis.