In vitro studies with primary calvarial osteoblasts from rodents indicated that IL-17 inhibited osteoblast differentiation through the inactivation of the WNT pathway.80–82 Also, IL-17 deficient mice developed more periosteal bone than wild type animals in an induced arthritis model.82 Furthermore, overexpression of IL-17 from the skin, leads to systemic bone loss due to osteoblast inactivation through WNT pathway inhibition in psoriasis mouse models. The gene discussed is IL17A; the disease is Arthritis.