Animal studies have shown that a high GC dose stimulates 24-hydroxylase activity and moderately reduces 1-alpha-hydroxylase activity in the kidneys.22 46–48 Functional cooperation between the GC receptor, the transcription factor C/EBPβ and the vitamin D receptor has been observed that increases 24-hydroxylase transcription.49 Thus, the experimental data allow to formulate the concept that vitamin D deficiency develops with long-term GC therapy due to accelerated 25(OH)D catabolism. The gene discussed is VDR; the disease is vitamin D deficiency.