When Abcd1 and/or Abcd2 genes are silenced in mouse primary astrocytes, X-ALD biochemical hallmarks are present (decreased C24:0 β-oxidation, increased C26:0 level), but so are redox imbalance and pro-inflammatory features (increased cytokines expression and nitric oxide production) [121]. This evidence concerns the gene ABCD1 and adrenoleukodystrophy.