Under pathological conditions, duplication and deletion upstream of LMNB1 are two different mechanisms of ADLD to result in the increasing expression and accumulation of laminB1 (Mezaki et al., 1984; Giorgio et al., 2015; Padiath, 2015; Nmezi et al., 2019). The gene discussed is LMNB1; the disease is adult-onset autosomal dominant demyelinating leukodystrophy.