The actions of 1,25(OH)2D via VDR involve stimulation or suppression of gene activity, often quite distant from the transcription start site.(7) Global deletion of the Vdr (Vdr−/− mice) produced a phenocopy of the congenital human disease vitamin D dependent rickets type 2A (VDDR2A), also known as hereditary vitamin D resistant rickets (HVDRR).(8). Here, VDR is linked to X-linked dominant hypophosphatemic rickets.