It has been widely recognized that an abnormal activation of CD4+ lymphocytes producing proinflammatory cytokines (i.e. interleukin (IL)-8, IL-6, IL-17, and tumour necrosis factor (TNF)-α) has a role in RA [6–8], but current studies have also shown that γδ T lymphocytes promote the onset and progression of RA [9]. This evidence concerns the gene IL17A and rheumatoid arthritis.