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Background: One of the most prevailing hypotheses of schizophrenia implicates the dopaminergic system. Positron Emission Tomography (PET) studies have consistently reported increased presynaptic dopamine synthesis capacity (DSC) in individuals with schizophrenia. Interestingly, striatal hyperdopaminergia has also been shown to precede the onset of psychosis and to be associated with symptom severity. Although current evidence suggests that dopaminergic dysregulation has at least a state component, the evidence for the trait component is still ambiguous. This highlights the need for studies in a homogenous population of individuals with shared etiological genetic risk factors. Over the last fifteen years, it has been well established that 22q11 deletion is one of the most important genetic risk factors for the development of schizophrenia. Individuals with 22q11 deletion are at increased genetic risk for psychosis, reaching a prevalence for schizophrenia spectrum disorders of 23.53% in adults between 18 and 26 years old and 41% in individuals above 26 years old 30% for psychotic disorder. This mutation accounts for 1% -2% of sporadic cases of schizophrenia. The aim of our study was to investigate dopamine (DA) function in individuals with 22q11 deletion.