For instance, in a case of ADLD, a deletion upstream of the LMNB1 gene eliminates the TAD and its boundary causing ectopic interactions between at least three forebrain enhancers and the LMNB1 promoter leading to Lamin B1 overexpression, as observed in other typical ADLD cases (Brussino et al., 2010; Giorgio et al., 2015). This evidence concerns the gene LMNB1 and adult-onset autosomal dominant demyelinating leukodystrophy.