Notably,in vivo administration of a pan-ROCK inhibitor, fasudil (which blocks both ROCK1 and ROCK2 activity), or a ROCK2 selective inhibitor resulted in decreased IL-17 and IL-21 production, diminished autoantibody production, and attenuation of arthritis in both spontaneous and induced models of RA23,25, supporting a role for the RhoA–ROCK pathway, and in particular the ROCK2 isoform, in RA. This evidence concerns the gene ROCK2 and rheumatoid arthritis.