The membrane protein Nogo-A and its receptor NgR have been extensively characterized for their role in restricting axonal growth, regeneration, and plasticity in the central nervous system. Recent evidence suggests that Nogo and NgR might constitute candidate genes for schizophrenia susceptibility. In this article, we critically review the possibility that dysfunctions related to Nogo-A and NgR might contribute to increased risk for schizophrenia. To this end, we consider the most important insights that have emerged from human genetic and pathological studies and from experimental animal work. Furthermore, we discuss potential mechanisms of Nogo/NgR involvement in neural circuit development and stability, and how mutations or changes in expression levels of these proteins could be developmental risk factors contributing to schizophrenia.