The difference is that this was accomplished mainly by perturbing the conventional differentiation of Th17 cells.164 In the context of RA, the NF-κB signaling pathway activated by IL-6 and TNF-α from the inflammatory milieu triggers the sustained expression of miR-34a, reducing the levels of the transcription factor FoxP3, which is specifically expressed in Tregs and critically governs their development and function.165 Furthermore, some miRNAs display simultaneous effects on the differentiation of Th17 cells and Tregs. Here, FOXP3 is linked to rheumatoid arthritis.