These inhibitors down‐regulate T cell activation, increase negative T cell signaling, and increase the Treg/Th17 ratio.[37] Human dental follicle‐derived MSCs co‐incubated with IFN‐γ in vitro were shown to enhance Treg increase in RA patients further, increase T cell activity in RA patients, and inhibit T cell apoptosis.[38] He et al. This evidence concerns the gene IFNG and rheumatoid arthritis.