Recent studies in Rheumatoid arthritis (RA) have shown that iron metabolism disorders caused by iron overload and impaired transferrin function lead to the production of reactive oxygen species; ferroptosis-associated pathways, such as dysregulation of the System Xc<sup>-</sup>/GPX4 axis dysregulation, NCOA4-mediated ferritin autophagy, endoplasmic reticulum stress and ferroptosis pathway crosstalk; as well as ferroptosis plays a regulatory role in a variety of immune cells, such as T-cells, B-cells, macrophages, etc., which collectively constitute a complex disease regulatory network in RA. This evidence concerns the gene GPX4 and iron metabolism disease.