These findings gain significance in the context of Autosomal Dominant Leukodystrophy (ADLD), a remarkably rare and fatal neurodegenerative disorder characterized by the overexpression of Lamin B1 (LMNB1) due to genetic anomalies such as LMNB1 gene duplications or deletions. This evidence concerns the gene LMNB1 and adult-onset autosomal dominant demyelinating leukodystrophy.