HDACs are well-known to catalyze the deacetylation of various proteins, thereby affecting their stability at post-translational levels.42 Studies have shown that HDAC3 can interact with RCAN1 and increase RCAN1 protein stability by inhibiting its poly-ubiquitination.76 HDAC3 controls the stability of cyclin A by altering its acetylation level.77 In our study, we found that FOXK1 was another substrate of HDAC3 in RA-FLSs. Here, FOXK1 is linked to rheumatoid arthritis.