RAN and mild neurocognitive disorder: These limitations, along with lack of understanding of the physiological roles of regulators of Ran GTPase in MND pathogenesis, highlight the need for novel loss-of-function mouse models of MND that perturb Ran GTPase and its substrates to elucidate the molecular and cellular mechanisms underlying the normal biology and disease processes that occur in motoneurons (Matus et al., 2014).