Its main active ingredient, total dajizin triterpenes, reduces the expression of ACSL4 in the rat model of RA, increases the expression of glutathione and GPX4, and upregulates Kelch-like ECH-associated protein 1 and HO-1 in the Nrf2/HO-1/GPX4 pathway, indicating that total dajizin triterpenes can inhibit cell aberrant ferroptosis by suppressing lipid peroxidation and thus exert therapeutic anti-RA effects [168]. This evidence concerns the gene NFE2L2 and rheumatoid arthritis.