There is ample evidence suggesting that epigenetic mechanisms may mediate the development of chronic inflammation by modulating the expression of proinflammatory cytokines such as TNF and interleukins and the autocrine and paracrine activation of the transcription factor NF‐kB 63, which we have recently described as being activated in the spinal cord of the mouse model of X‐ALD 62 and peripheral blood of pure AMN patient samples 59. This evidence concerns the gene NFKB1 and adrenomyeloneuropathy.