A recent study showed that the peripheral Vγ9Vδ2 T cells isolated from RA patients upregulated their expression of APC-specific molecules HLA-DR and CD80/86 when stimulated with IPP in vitro and presented soluble antigens and synthetic peptides to CD4+ T cells and B cells, thus contributing to sustained activation of CD4+ T cells and being associated with RA onset and disease progression [14]. The gene discussed is CD4; the disease is rheumatoid arthritis.