Schizophrenia is complex neurological disease that is present in 1% of the general population. It is known as a multifactorial disease because of the simultaneous influence of genetic and environmental factors. Some of the symptoms that are recognized are hallucinations, delusions, loss of energy and motivation and cognitive dysfunctions like working memory dysfunction and dysfunctions in learning. A major problem in treating schizophrenia is its heterogeneity and patients do not respond the same to the same treatment. There is also little to no effect in treating cognitive dysfunction with available medications. We still have limited knowledge of the core of pathology of disease and more research are needed to find the best treatment. In the past years lots of research was performed on genetic risk factors for schizophrenia, and one of the most researched genetic factors is the DTNBP1 gene. The DTNBP1 gene encodes for dysbindin-1 protein. In the brain, dysbidnin-1 is mostly expressed in the hippocampus and prefrontal cortex. Studies on post-mortem schizophrenia cases found that there is a decrease in dysbindin-1 expression in brain. These suggest the involvement of dysbindin-1 in the pathology of disease. Dysbindin-1 is known to be a component of the BLOC-1 complex in brain and therefore regulates several functions in the brain including vesicular trafficking following by regulation of neurotransmitter release, neural growth, and transcriptional regulation. Studies on “sandy” mice, with a mutation in the Dtnbp1 gene also show promising results in its involvement in developing schizophrenia-like symptoms. Researching dysbindin-1 and other genetic risk factors functions in the brain and their binding partners is important in finding new potential targets for future treatment of schizophrenia.