For instance, overexpression of PRDX5 in human tendon cells induces apoptosis following H2O2 treatment [15], up-regulation of PRDX5 has been reported in osteoarthritic cartilage and in TNF-α or IL-1β treated cartilage explants from patients with osteoarthritis [16], and PRDX5 was proven to be an anti-fibrotic effector that sustains renal physiology by inhibiting stat3 activation in rat kidney interstitial fibroblast cells [17]. This evidence concerns the gene PRDX5 and osteoarthritis.