In slow progressing B6 Col4a3−/− mice, bone Nfat1 mRNA expression was significantly increased, whereas lifelong DMP1 overexpression in B6 Col4a3−/−/DMP1TG mice prevented this increase (Fig. 5f), suggesting that lack of DMP1-mediated suppression of NFAT-induced Fgf23 transcription contributes to FGF23 excess in CKD. The gene discussed is FGF23; the disease is chronic kidney disease.