Finally, a recent study has achieved to abrogate the ADLD-specific phenotypes with the use of siRNA treatment (non-duplicated allele by ASP-siRNA used may reduce the amount of LMNB1 without excessively downregulating the gene) in ADLD fibroblasts, in murine oligodendrocytes overexpressing human LMNB1, and neurons directly reprogrammed from patients' fibroblasts, providing an effective therapeutic strategy for ADLD treatment [53]. The gene discussed is LMNB1; the disease is adult-onset autosomal dominant demyelinating leukodystrophy.