Although ADLD has been known to be the result of genomic duplication of the lamin B (LMNB) gene, chromosomal rearrangements affecting TAD boundaries have been demonstrated to lead to enhancer adoption and eventual LMNB overexpression.44 Furthermore, TAD boundary disruptions and mutations in CTCF binding sites have been implicated in enhanced oncogene expression, through the formation of abnormal enhancer–promoter interactions.45, –47. This evidence concerns the gene LMNB1 and adult-onset autosomal dominant demyelinating leukodystrophy.