In summary, the present study explored the potential mechanism of MiR-128-3p in RA, with the results of MiR-128-3p were significantly increased, the T cells and the NF-κB signaling pathway were activated, while down-regulating the expression of MiR-128-3p significantly suppressed the activation of T cells and the NF-κB signaling pathway, which was mediated by TNFAIP3, and further relieved the symptom of RA. Here, NFKB1 is linked to rheumatoid arthritis.