As a whole, our data suggest that the attributable effect of the CYP1B1, CYP2C9, ESR1, ESR2, SHBG, and FcγR3A loci to modulate the risk of developing bone erosions in RA patients might be dependent on the presence of either missense or intronic polymorphisms that affect the immune responses to a greater or lesser extent. Here, FCGR3A is linked to rheumatoid arthritis.