This is likely to be related to dual anti-CCP2/CCP3 positivity reflecting an expanded ACPA repertoire (i.e. different antigenic targets/ACPA fine specificity being detected) and suggests that in anti-CCP2+ at-risk individuals, anti-CCP3 antibodies may be identifying a more advanced stage of autoimmunity driving the onset of subclinical and later clinical inflammation [29, 30]. This evidence concerns the gene PRTN3 and Autoimmunity.