Belsky et al.13 recently delineated a series of empirical requirements, or steps, for convincingly establishing evidence of differential susceptibility to environmental influence, that is, individual differences in plasticity. The first concerns the application of conventional statistical criteria for evaluating genuine moderation of a putative environmental influence by an organismic plasticity or susceptibility factor,15 including genotype, with some emphasis on excluding interactions with regression lines that do not cross (sometimes referred to as removable interactions). The next steps distinguish differential susceptibility from person–environment correlations, including Gene–Environment ones, which may reflect evocative effects of person characteristics on environmental experiences and from diathesis–stress models. If the (genetic) susceptibility factor and the (problematic) outcome are related, diathesis–stress is suggested. The specificity of the differential-susceptibility effect is demonstrated if the model is not replicated when other (genetic) susceptibility factors (that is, moderators) and outcomes are used.16, 17 Differential susceptibility is thus demonstrated when the moderation reflects a crossover interaction that covers both the positive and the negative aspects of the environment, with the positive typically (and unfortunately) represented by the mere absence of adversity. The
