We hypothesize that the milieu within the inflamed synovium of RA patients favors the induction of miR-31, on the one hand by a repeated auto-antigenic stimulation inducing the expression of T-bet and IFN-γ, and on the other, by IL-7 expression (73) which represses FOXO1 (48), thereby arresting proinflammatory Th cells in the inflamed tissue, where they receive survival signals that counteract immunosuppressive therapies and promote inflammation (4). This evidence concerns the gene IFNG and rheumatoid arthritis.