Serotonergic systems have been reported to mediate the control of aggression and/or impulsivity in humans and to be involved in suicidal behavior. Neurochemical studies showing serotonergic dysfunction in suicide appear to support the functional alteration of serotonergic systems due to gene polymorphisms. Knock-out mice of the 5HT1B receptor gene have been reported to result in increased aggression. We hypothesized that the 5HT1B receptor-mediated serotonergic dysfunction was implicated in suicide through disinhibition of aggression and/or impulsivity. To explore this hypothesis, we examined the association between suicide victims who completed suicide and the 5HT1B receptor gene G861C polymorphism. No significant differences in genotype distribution and allele frequencies were found between suicide victims and controls. Though there is the possibility of failing to detect small effects, these results show no evidence of an association between the 5HT1B receptor gene G861C polymorphism and suicide victims in a Japanese population and indicate that it is unlikely that the 5HT1B receptor is implicated in the susceptibility to suicide.