It can therefore be hypothesized that increased Prevotella copri in RA may also consume Trp without producing AhR activators through specific pathways, thus preventing the physiological accumulation of activators such as Kyn and the subsequent activation of AhR, which in turn affects FoxP3 expression, leading to reduced population and impaired function of Treg cells. This evidence concerns the gene FOXP3 and rheumatoid arthritis.