We measured the effects of type I (IFN‐α) IFN, elevated in both RA and SLE, on the functions of healthy neutrophils incubated in vitro in the absence and presence of proinflammatory cytokines typically elevated in inflammatory diseases [tumour necrosis factor (TNF‐α), granulocyte–macrophage colony‐stimulating factor (GM‐CSF)]. This evidence concerns the gene IFNA1 and rheumatoid arthritis.