showed that IL-37 could attenuate TNF-α-induced RA-FLS juxtaposition by inhibiting the NF-κB/GSDMD signaling pathway, reduce the expression of the inflammatory factors IL-18 and IL-1β in the cell supernatant, inhibit the proliferation of FLS, and attenuate the inflammatory response of RA joints, which serves as a therapeutic purpose for the prevention and treatment of RA (296). This evidence concerns the gene NFKB1 and rheumatoid arthritis.