When it comes to Tregs, we know that the TNF-α cytokine is capable of compromising the proper function of this population in rheumatoid arthritis, and one of the mechanisms is to reduce the phosphorylation of the FoxP3 transcription factor so that the treatment with anti- TNF contributes to the reestablishment of the function of these cells, reversing this effect and further reducing the action of IFN-γ and IL-17 and promoting a balance between cell profiles [44]. Here, IFNG is linked to rheumatoid arthritis.