Consistently, the recovery of tremors and the decreasing of periaxonal vacuoles in the dop1a-null-mutant rats, as well as the recovery of nystagmus/ataxia in IV-2, both indicated that there might be other pathways that could complement the dysmyelinogenesis of PLP/MAG partially in adulthood. The gene discussed is DOP1A; the disease is Nystagmus.