Overexpressed ICAM2 partly reverses the inhibitory impact of ATT on the proliferation, migration and invasion, and the apoptosis‐inducing effect of ATT in RA‐FLSs suggesting that an ICAM2‐independent mechanism may exist for the regulation of abnormal functions in RA‐FLSs by ATT. Here, ICAM2 is linked to rheumatoid arthritis.