With CLCN2-related leukodystrophy the situation is more complex: Clcn2 disruption in oligodendrocytes led cell-autonomously to myelin vacuolization, whereas additional deletion in astrocytes, which form gap junction–connected syncytia with oligodendrocytes (43, 44), was required to achieve the same extent of vacuolization observed with global Clcn2 disruption. Here, CLCN2 is linked to leukodystrophy.