Schizophrenia is a complex syndrome associated with diverse clinical, cognitive, and neurobiological features that can vary substantially from one patient to the next. Identifying the core mechanisms underlying this syndrome and improving patient outcomes has been a major challenge. In this talk, I will present my work using a pharmacological probe in humans to examine one compelling etiologic model of schizophrenia, the NMDA receptor dysfunction model. I will then discuss my work using functional genomics to systematically examine which aspects of brain development are affected by genetic risk for schizophrenia and related disorders. Finally, I will present initial evidence suggesting that schizophrenia may be better conceptualized as a cluster of syndromes, with related but dissociable etiologies. I will close by outlining my future research program aimed at identifying biologically valid subgroups of schizophrenia patients, with implications for how and when to intervene during development.