Accordingly, in human X-ALD monocytes, the metabolic defects such as accumulation of VLCFA and their degradation by peroxisomal β-oxidation are comparable to those found in Abcd1/Abcd2 double-deficient rather than Abcd1-deficient peritoneal macrophages. This evidence concerns the gene ABCD1 and X-linked adrenoleukodystrophy.