Multi-ancestry genome-wide association analyses provide insights into the genetic basis of Hashimoto's thyroiditis.

Over the past two decades, prevention science has increasingly shifted from asking whether interventions work to understanding how they work. This transition has been driven, in part, by the National Institutes of Health's experimental therapeutics framework, which emphasizes identifying and testing specific mechanisms hypothesized to underlie psychopathology (Zucker et al., ). Rather than focusing solely on symptom reduction, this approach evaluates whether modifying targeted neurobehavioral processes that subserve social and emotional functioning alters risk trajectories. As a result, considerable progress has been made in identifying mechanisms that confer vulnerability to child and adolescent psychopathology, advancing the development and precision of mechanism‐focused preventive interventions. However, identifying a mechanistic target is only one dimension of precision prevention. An equally important question is whether interventions are differentially effective depending on when in development they are delivered. This reflects the premise that neurobehavioral systems follow dynamic developmental trajectories that may constrain or enhance their capacity for change at different points in time. Here, we propose that developmental timing represents a critical, yet often overlooked, dimension of mechanism‐based prevention, such that interventions should be designed not only to target the appropriate mechanism, but also to capitalize on developmental periods during which that mechanism is most malleable and most likely to alter long‐term trajectories. This perspective builds on the premise that neurobehavioral mechanisms do not emerge or mature uniformly across development. Rather, converging research suggests that different neurobehavioral systems exhibit distinct developmental trajectories characterized by periods of heightened plasticity. Consequently, different mechanisms are likely to possess distinct developmental windows of opportunity during which they are especially amenable to intervention. For example, early childhood has been identified as a particularly important period for shaping stress‐response systems and emotion regulation through caregiver‐child interactions (Gee, ), whereas middle childhood and adolescence may represent key windows for interventions targeting executive control as prefrontal systems mature and social‐affective processes, including sensitivity to peer evaluation and social reward, increase (Blakemore & Mills, ; Selemon, ). These developmental transitions may represent windows during which interventions can produce larger and more enduring effects. Rather than viewing developmental timing as a secondary design consideration, we suggest that it should be considered alongside mechanistic target selection when designing preventive interventions. Just as neurobehavioral mechanisms emerge and mature at different periods across development, their capacity to be experimentally altered may likewise be developmentally constrained. From this perspective, developmental windows may determine not only the magnitude of intervention effects, but also whether the targeted neurobehavioral mechanism is sufficiently developmentally malleable to be modified by intervention.