Suicide is considered a major preventable public health problem and is the 10th leading cause of death in the United States for all age groups combined. It is generally accepted that suicide marks the tragic endpoint of a highly complex behavior shaped by social, developmental, and neurobiological factors that translate into a predisposition for the act itself. For example, altered serotonergic activity in the prefrontal cortex, which appears to be partially independent of the changes observed in major depression, is thought to play an important role (1, 2). Furthermore, the concordance rate for serious suicide attempts in monozygotic twins has been reported to be up to 17-fold greater than in dizygotic twins, and heritability estimates for serious suicide attempts are estimated to be as high as 55% (2). On the other hand, recent genome-wide association studies of nearly 9,000 individuals diagnosed with a mood disorder, approximately one-third of whom had a history of attempted suicide, effectively ruled out common genetic variants and polymorphisms of large effect (3). Following this approach, much larger cohorts will be required in order to gain insight into what appears to be a highly polygenic risk architecture.