We speculate that it may be because of the inhibition of HDAC6 activity, as HDAC6 regulates α-tubulin acetylation and facilitates transportation of degradable proteins from the aggresome to the lysosome.26, 27 In addition, an HDAC6 inhibitor resulted in α-tubulin hyperacetylation, disruption of the interaction between HDAC6 and dynein, and an increase in the delivery of ubiquitinated proteins to the proteasome.28 Our results showed that in RA-FLS, MPT0G009 inhibited HDAC6 activity and also reduced the levels of HDAC3 by proteasomal-mediated degradation. The gene discussed is HDAC6; the disease is rheumatoid arthritis.