Interestingly in fact, anti-CCP2-positive UA patients who will develop RA display reactivity against a significant larger number of citrullinated epitopes, namely vimentin, fibrinogen and α-enolase, with respect to anti-CCP2-positive patients not evolving toward RA at one year of follow up, thus postulating a very distinct immunological reactivity profile at disease onset [33]. The gene discussed is AGBL2; the disease is rheumatoid arthritis.