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. This evidence concerns the gene HLA-DRB5 and systemic lupus erythematosus.