Our findings showed that prednisolone administration led to a decrease in the level of 25-dihydroxyvitamin D, a vitamin D status marker, in the serum along with an impaired bone synthesis of key components of the vitamin D auto-/paracrine system, VDR and CYP27B1, and consequently induced hypophosphatemia and hypocalcaemia and increased the activity of alkaline phosphatase in the serum and reduced content of mineral components in bone tissue. The gene discussed is CYP27B1; the disease is hypophosphatemia.