From this study we can conclude that the contribution of HLA-SE alleles and smoking prior to RA increased closer to disease onset and were moderate, but in combination with the most prevalent antibodies (CEP-1/Eno5-21, Fibß36-52, and CCP-1/Fil307-324) aside from anti-CCP2 antibodies, the relative risk for disease development was highly increased. The gene discussed is AGBL2; the disease is rheumatoid arthritis.