Importantly, blockade of CRP signaling with neutralizing antibodies to CD32 or CD32/CD64, but not to CD64 alone, largely inactivated CRP-induced phosphorylation of p38, IκBα, IKK, and p65 signaling (Figure 5A), revealing a primary role for CD32-p38/ NF-κB signaling in CRP-mediated activation of RA-FLS. The gene discussed is CRP; the disease is rheumatoid arthritis.