In this study, we established a rat model of RA to examine the biological mechanisms by which BM‐MSC‐extracted Evs participate in the inflammation of RA and found that miR‐34a from BM‐MSC‐derived Evs could regulate the function of synovial fibroblasts in RA by inhibiting cyclin I and activating the ATM/ATR/p53 signalling pathway. The gene discussed is ATR; the disease is rheumatoid arthritis.