However, because of failure to replicate genetic association studies [24], a lack of causal variants with a notable impact on disease risk that might contribute to schizophrenia [25], and methodological difficulties in postmortem brain research due to heterogeneity of tissues with respect to biochemical parameters, lifetime history of medications and physiological status at the time of death [26], it remains unclear how dysbindin-1 functions as a susceptibility gene for these disorders. The gene discussed is DTNBP1; the disease is schizophrenia.