In the present study, we propose a novel mechanism to explain coincident increases in LCN2 and FGF23 soon after kidney injury,32 and the strong independent association between elevated levels of FGF23 and inflammatory markers.33 We hypothesized that bone is a target of kidney-secreted LCN2 and that increased LCN2 stimulates bone production of FGF23 in CKD. The gene discussed is LCN2; the disease is chronic kidney disease.