Abstract: Recent research with both humans and rhesus monkeys has provided compelling evidence of gene–environment (GxE) interactions throughout development. For example, a specific polymorphism (“short” allele) in the promoter region of the serotonin transporter (5-HTT) gene is associated with deficits in neurobehavioral functioning during infancy and in poor control of aggression and low serotonin metabolism throughout juvenile and adolescent development in monkeys who were reared with peers but not in monkeys who were reared with their mothers and peers during infancy. In contrast, monkeys possessing the “long” allele of the 5-HTT gene exhibit normal neurobehavioral functioning, control of aggression, and serotonin metabolism regardless of their early social rearing history. One interpretation of these GxE interaction data is that the “long” 5-HTT allele somehow confers resiliency to adverse early attachment relationships on those individuals who carry it (“good genes”). An alternative interpretation of the same data is that secure attachment relationships somehow confer resiliency to individuals who carry alleles that may otherwise increase their risk for adverse developmental outcomes (“maternal buffering”). These two interpretations are not mutually exclusive, but the difference in their respective implications for developing prevention and even intervention strategies is considerable. Moreover, the allelic variation seen in certain genes in rhesus monkeys and humans but apparently not in other primate species may actually contribute to their remarkable adaptability and resilience at the species level.