The article challenges the traditional diathesis-stress framework in psychiatric genetics, which views individuals as particularly vulnerable to adversity due to their genetic makeup. Instead, it proposes a 'differential susceptibility' framework, suggesting that individuals with certain genetic variations are more susceptible to both positive and negative environmental influences. The authors review recent findings involving monoamine oxidase-A (MAOA), 5-hydroxytryptamine-linked polymorphic region polymorphism (5-HTTLPR), and dopamine receptor D4 (DRD4) to illustrate how these 'vulnerability genes' might be better conceptualized as 'plasticity genes.' They argue that these genes make individuals more susceptible to environmental influences, which can be either beneficial or detrimental. The article emphasizes the need for research that measures environmental support and positive functioning in addition to adversity and negative outcomes, to fully understand the differential susceptibility hypothesis. The authors conclude by calling for changes in research practices to better capture the complexity of gene-environment interactions and to avoid mischaracterizing individuals as simply vulnerable to adversity.The article challenges the traditional diathesis-stress framework in psychiatric genetics, which views individuals as particularly vulnerable to adversity due to their genetic makeup. Instead, it proposes a 'differential susceptibility' framework, suggesting that individuals with certain genetic variations are more susceptible to both positive and negative environmental influences. The authors review recent findings involving monoamine oxidase-A (MAOA), 5-hydroxytryptamine-linked polymorphic region polymorphism (5-HTTLPR), and dopamine receptor D4 (DRD4) to illustrate how these 'vulnerability genes' might be better conceptualized as 'plasticity genes.' They argue that these genes make individuals more susceptible to environmental influences, which can be either beneficial or detrimental. The article emphasizes the need for research that measures environmental support and positive functioning in addition to adversity and negative outcomes, to fully understand the differential susceptibility hypothesis. The authors conclude by calling for changes in research practices to better capture the complexity of gene-environment interactions and to avoid mischaracterizing individuals as simply vulnerable to adversity.