Whilst neutrophils from healthy controls and clinically active RA bind at similar levels to fibronectin in vitro, significantly fewer cells adhered when they were isolated from patients in clinical remission – these observations were linked to reductions in the expression of L-selectin and αL-integrin on neutrophils following anti-TNFα therapy (Dominical et al., 2011). This evidence concerns the gene FN1 and rheumatoid arthritis.