Beyond its anti-tumor effects, abundant tumor necrosis factor-α (TNF-α) in the RA synovial environment has been found to elevate the expression of cleaved caspase-3 and GSDME-N, leading to synovial cell pyroptosis and promoting the secretion of inflammatory factors, thereby exacerbating arthritis severity [131,132]. This evidence concerns the gene TNF and arthritic joint disease.