A recent case report of a patient with severe ankylosing spondylitis who did not react to VitD supplementation [9] showed severe VDBP deficiency, and consequently, in a significant decrease in VitD-responsive CYP24A1 and VitD metabolites such as 25(OH)D3 and 1,25(OH)2D3, due to homozygous deletion of the GC gene. The gene discussed is GC; the disease is hyperinsulinemic hypoglycemia, familial, 4.