Selenium deficiency is well correlated with the development of Kashin–Beck osteoarthropathy,[40] an endemic disabling osteoarticular disease; whereas selenium supplementation benefits the prevention of Kashin–Beck in children.[41] Selenophosphate synthetase 1, an endogenous selenium donor, is essential for the regulation of selenium metabolism, while its deficiency exacerbates OA development through oxidative stress injury.[42] Subsequent studies will look into the roles of other sirtuins (SIRT5 or SIRT7) and selenoprotein (TXNRD1/2) in OA development. This evidence concerns the gene TXNRD1 and selenium deficiency.