The production of IL-17 and IL-21 by SLE T cells is furthermore amenable to inhibition by statins (which, by blocking RhoA prenylation, can interfere with RhoA activation), a pan-ROCK inhibitor, or a selective ROCK2 inhibitor, further supporting a link between the RhoA–ROCK pathway and T cell dysfunction in this disease (Rozo, Salmon, and Pernis, unpublished observations). This evidence concerns the gene IL17A and systemic lupus erythematosus.