Overexpression of Abcd2 in whole nervous system or in fibroblasts from Abcd1-deficient mice or from X-ALD patients is shown to restore peroxisomal β-oxidation and to reduce excessive accumulation of VLCFA [34], [38], [40], [41], [42], [43]. This evidence concerns the gene ABCD2 and X-linked adrenoleukodystrophy.