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The primary etiology of FXS involves the expansion of CGG trinucleotide repeats in the 5 untranslated region of the FMR1 gene, typically ranging from 55 to 200 repeats in premutation carriers and exceeding 200 repeats in full mutation alleles (216)

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The regular vitamin D metabolic profiles illustrated with either wild-type mouse VDR or VDR null mice transgenic for the wild-type human VDR, but not the ligand binding-defective form of the protein, this suggests the essential roles of VDR on VD metabolism 25