We studied Col4a3−/− mice that recapitulate many features of human CKD including progressive loss of kidney function, alterations of bone and mineral metabolism, elevations of circulating FGF23 levels, development of LVH in slow progressing B6 Col4a3−/−, and shortened lifespan.29–32 We demonstrate that CKD leads to significant alterations in osteocytes, including apoptosis, reduced DMP1 expression and activation of the calcium-dependent NFAT signaling that contributes to increased FGF23 transcription. The gene discussed is COL4A3; the disease is chronic kidney disease.