Anticitrullinated protein antibodies (ACPAs) constitute a class of 
autoantibodies found in 60-70% of patients with rheumatoid arthritis (RA). The 
most common test for ACPA positivity is based on the occurrence of antibodies 
that bind to circular citrullinated peptides, so-called CCP, some of which are 
derived from endogenously citrullinated proteins, like filaggrin. Several lines 
of evidence suggest that these autoantibodies may confer pathological reactions. 
They appear years before onset of clinical disease and are associated with worse 
prognosis and a more erosive disease. Their presence correlates with the most 
prominent genetic risk factors for RA development, and they were recently 
described to mediate relevant biological functions such as activation of 
complement system and induction of osteoclastogenesis. The development of new 
drugs that specifically target these autoantibodies is an appealing and novel 
approach. Herein, we briefly review the autoimmune condition of RA, 
characterized by the presence of ACPA, and we describe how the neutralization of 
autoantibodies might become a novel pharmacological principle.