By applying this panel to large case-control cohorts for RA and SLE, we revealed that the risk effects at HLA-DRB3, HLA-DRB4, and HLA-DRB5 were neither superior to nor independent of the HLA-DRβ1 amino-acid model in RA and SLE. The gene discussed is HLA-DRB1; the disease is rheumatoid arthritis.