As classical anti-inflammatory treatment paradigms including application of IFNβ were unable to stop the neuroinflammation in X-ALD patients [67], pharmacological inhibition of factors involved in trans-endothelial migration across the BBB such as CCR2 or CXCL8 might be of interest in the context of developing alternative treatment strategies for the inflammatory cerebral form of X-ALD. The gene discussed is CXCL8; the disease is X-linked adrenoleukodystrophy.