Interestingly, in antigen-induced experimental arthritis, IL-6 has been shown to function upstream of IL-17, but has also been shown to be a downstream target of IL-17A, and the combination of IL-6 and IL-17A synergistically generated a positive IL-6 expression feedback loop that resulted in excessive IL-6 signaling through the soluble IL-6 receptor (IL-6R) signaling pathway [72]. The gene discussed is IL17A; the disease is arthritic joint disease.