Different mechanisms have been suggested to explicate the impairment of PON-1 activity in RA patients, including the enhanced generation of reactive oxygen species [39] compositional changes of HDL [23], inhibitory effect of proinflammatory cytokines on the liver synthesis of PON-1 [40], and genetic polymorphisms of the PON-1 gene [41,42]. The gene discussed is PON1; the disease is rheumatoid arthritis.