Collapsin response mediator proteins 1−5 (CRMPs1−5) are a family of cytosolic proteins that coordinate neuronal migration, axonal guidance, dendritic organization, dendritic spine development and synaptic plasticity (reviewed in Khanna et al.1and Quach et al.2). Members of the CRMP family are reported to be involved in the pathogenesis of various neuronal disorders. For instance, proteomic, genomic and translational approaches linked the CRMP1 gene with chronic, negative symptoms of schizophrenia and severe major depression.3 Mice lacking CRMP1 manifest hyperactivity, impaired learning and memory, and impaired prepulse inhibition behavioral abnormalities related to schizophrenia.4 Genetic association and linkage studies pointed to CRMP2 as a liability gene for schizophrenia, autism, alcohol dependence, depression and bipolar disorders.5, 6, 7, 8, 9, 10 Mice with brain-specific Crmp2 deletion exhibited behavioral deficits in locomotor activity, sensorimotor gating, social behavior, and spatial learning and memory.11 Maternal autoantibodies against CRMP1 and CRMP2 were found in children with autism spectrum disorders that displayed core deficits in communication and reciprocal social interaction as well as repetitive or stereotypical behaviors.12 CRMP3-deficient mice display significant decreases in dendritic length and branching points, and an abnormal undulation of apical primary dendrites; these findings are recapitulated in the brain of Down syndrome where the expression of CRMP3 gene is also impaired.13 Little is known about the relationship between CRMP4 and neuropsychiatric disorders. However, mice lacking CRMP4 manifest impaired olfactory function and hyperactivity in the olfactory bulb and have increased levels of ionotropic glutamate receptors GluRs 1 and 2, which have been implicated in autism spectrum disorders and schizophrenia.14 CRMP5 knockout mice implicate this protein in dendritic development and synaptic plasticity in cerebellar purkinje cells,15 and CRMP5 autoantibodies were reported in patients with paraneoplastic neurological syndrome characterized by cerebellar ataxia and chorea. Therefore, understanding CRMP signaling has significant clinical implications.