ABCD2 expression is lacking in human fibroblasts; thus, the 10%–15% residual β‐oxidation in ALD is most likely due to ABCD3 (Wiesinger, Eichler, & Berger, 2015; Wiesinger, Kunze, Regelsberger, Forss‐Petter, & Berger, 2013). This evidence concerns the gene ABCD3 and adrenoleukodystrophy.