By contrast, adverse environmental conditions may act as social stressors that trigger or strengthen genetic effects for AUD; evidence points to an individual’s responsiveness or sensitivity to stressful conditions being influenced by genetic factors18. Nurturing environments conceptually may be placed at the other end of this spectrum, but have not been the focus of G–E studies of AUD. For example, Turkheimer et al.19 examined a continuum of socioeconomic conditions, showing different relationships for genetic and environment effects with intelligence when comparing impoverished and affluent family environments. Conversely, studies of GxE triggering mechanisms for AUD, as well as for major depression and aggression, have focused more on contextual variables like stressful life events and childhood maltreatment10,11. Two recent measured-gene studies identified significant interactions between genetic effects and childhood adversities (e.g., abuse, parental divorce or death, witnessed violence) in predicting AUD: Meyers et al.20 and Sartor et al.21 reported, respectively, an enhanced association of the ADH1B risk variant and a reduced association of the ADH1B protective variant with AUD under adverse childhood conditions. These studies are complemented by evidence suggesting strong main