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). The gene discussed is ABCD3; the disease is X-linked adrenoleukodystrophy.