Thus, VLCFA accumulation, due to mutations in ABCD1, may trigger the pathogenic cascade in X-ALD by oxidizing/inactivating the “energetic enzymes” of Krebs cycle and glycolysis, and leading to decreased levels of NADH and ATP, as shown in the spinal cords of X-ALD mice [10]. This evidence concerns the gene ABCD1 and X-linked adrenoleukodystrophy.