Recent studies suggest that reducing LMNB1 levels and restoring small molecules associated with nuclear abnormalities may prevent the occurrence and progression of the disease (Lin and Fu, 2009; Lin et al., 2014; Nmezi et al., 2020), and protein regulation may provide new therapeutic opportunities for ADLD (Giorgio et al., 2021). The gene discussed is LMNB1; the disease is adult-onset autosomal dominant demyelinating leukodystrophy.