Intriguingly, we have recently demonstrated that the ability of ES-62 to protect against IL-17-dependent Th1-associated autoimmune inflammation in the collagen-induced mouse model of arthritis reflected targeting of a complex (γδ T cell, DC and Th17 interactions) cellular network in which ES-62 suppressed both initiation of, and maintenance of ongoing, IL-17 responses (Pineda et al., 2012). The gene discussed is IL17A; the disease is Arthritis.