Specifically, the authors demonstrated that enhancing SCD1 expression and activity using an agonist for liver X receptor (LXR), a nuclear receptor which senses cholesterol and regulates the expression of lipid metabolism genes including Scd1 [20–23], partially normalized the accumulation of toxic saturated VLCFA levels in X-ALD fibroblasts and male Abcd1-deficient (Abcd1–/y) mice [19]. Here, ABCD1 is linked to X-linked adrenoleukodystrophy.