Comparison of survivin levels between smokers and non-smokers of RA and healthy subjects suggest that nicotine contributes to autoimmunity by inducing the non-exhausted PD-1−IL-7R+ CD8+ T cells resulting in the release of survivin, and that potentially presents a new mechanism for smoke-mediated RA pathogenesis (55). This evidence concerns the gene CD8A and rheumatoid arthritis.