Skin fibroblasts from ADLD patients, where LMNB1 was found to be overexpressed by ∼1.5–2 fold, displayed nuclear abnormalities that were much more subtle and did not reveal a mislocalization of LAP2β or nucleoporins (Ferrera et al., 2014). This evidence concerns the gene LMNB1 and adult-onset autosomal dominant demyelinating leukodystrophy.