Apart from mitochondrial injury, mitochondrial N-formyl peptides (mtNFPs) concentrations in the plasma of RA patients are elevated and induce enhanced NETs activity in neutrophils via the formyl peptide receptor 1 (FPR1)-dependent pathway, promoting the immune response of neutrophils and being an important link in the pathogenesis of RA (31). This evidence concerns the gene FPR1 and rheumatoid arthritis.