Glycine induces ferroptosis in RA-FLSs via S-adenosylmethionine (SAM)-associated methylation of GPX4 promoter, further enhancing ferroptosis efficacy by downregulating FTH1 expression.357 P53, one of the frequent mutated tumor-suppressing genes, is increased in activated RA-FLSs.358 In addition, ferroptosis caused by sulfasalazine has a dual role. The gene discussed is TP53; the disease is rheumatoid arthritis.