Overexpression of ABCD2 has been shown to functionally compensate for the impairment in peroxisomal β-oxidation and VLCFA accumulation resulting from ABCD1 deficiency in human X-ALD fibroblasts and in Abcd1-deficient mice [29]–[31]. The gene discussed is ABCD1; the disease is X-linked adrenoleukodystrophy.