Since we previously suggested the involvement of PAI-1 in trabecular bone loss and delayed bone repair induced by a diabetic state and glucocorticoid excess in mice [8–11], and a diabetic state and glucocorticoid excess induce a chronic inflammation state and excessive oxidative stress, the pathogenesis of CKD-MBD may markedly differ from the pathophysiology of bone loss induced by diabetes and glucocorticoid excess. The gene discussed is SERPINE1; the disease is diabetes mellitus.