Herein, we specify a program of study for intervention researchers to pursue that may aid in accelerating the empirical specification of mechanisms of change in these interventions. First, using the wide range of existing interventions and with newly developed interventions that show promise, we suggest that clinical scientists in this field begin to Inhibitors,research,lifescience,medical focus on identifying predictors of individual difference in response (ie, moderators)

to these treatments. Such predictors may include factors such as gender, age, cognitive ability,129 or level of comorbid psychopathology. Such research would have implications for both future intervention research and immediate practice. It would permit the specification of models to empirically identify more promising mechanisms of response across treatments (eg, if more cognitively able youth respond better to CBT interventions, it may suggest that cognitive processing of intervention strategies may

be a pathways through which these interventions “work”). Just as importantly, Inhibitors,research,lifescience,medical though, it would directly aid in the development of markers to inform treatment selection for individual patients among the already-large Inhibitors,research,lifescience,medical and ever-growing body of putatively “evidence-based” psychosocial interventions. Such markers will be essential during the intermediate period, as the field begins to narrow down and optimize interventions based on developing research. Finally, it may be argued that answering “for whom” (see refs 8-10) any given treatment is likely to be most effective Inhibitors,research,lifescience,medical is particularly imperative in treatment research for ASD, given the heterogeneity of this clinical population.3,9,25,130 Relatedly, as the field begins to specify more precisely the neuroanatomical131 and electrophysiological93,94 processes underlying social dysfunction in ASD, it is crucial that such processes be included in this first phase. Notably, biomarkers such as a delayed N170 ERP component in response Inhibitors,research,lifescience,medical to faces95

L-NAME HCl may be used to begin to differentiate participants’ response to existing interventions based on theoretically sound principles. For instance, individual differences in N170 response may be used to determine whether or not processing deficits should be directly targeted in some participants and not others, in a treatment program seeking to improve social competence. Additionally, such biomarkers may be used to index change in neural processes in response to intervention,97 providing concrete measures of more systematic (and potentially enduring) change, as well as supporting the possibility of plasticity in neuropathological processes previously thought to be intractable.132 Second, we recommend the careful testing of proximal check details effects of these theorized mechanisms in lab-based settings.