IL17A and rheumatoid arthritis: In the present study, we demonstrated that i) peripheral blood T cells from RA patients showed an appreciable level of apoptosis, which was significantly increased upon stimulation with GalXM; ii) the observed apoptosis was related to GalXM-mediated induction of caspase-3 activation; iii) the major target population of GalXM-induced apoptosis was activated T cells producing IL-17A; iv) treatment with GalXM leads to significant impairment of IL-17A production; v) the GalXM-mediated effects include inhibition of STAT3, which is hyperactivated in RA.