HLA genotyping/matching of control and RA groups were not performed in our study because we have no direct evidence that known HLA polymorphisms that may (or may not) be involved in antigen-specific signaling in T cells, can have an effect on intrinsic BCR signaling events that are not the result of adaptive (antigen specific) B cell immune response [27], which is the major focus of our study. The gene discussed is BCR; the disease is rheumatoid arthritis.