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Atypical neural responses to face stimuli have been well-documented in children with autism spectrum disorder (ASD). However, much of this research excludes additional participant groups that are also impacted by varying degrees of ASD symptoms. In the current study, we investigated neural correlates of social information processing among children with ASD, as well as children with fragile X syndrome (FXS) and unaffected siblings of children with ASD (ASIBs). FXS is single gene disorder often characterized by intellectual impairment. Approximately 60% of preschoolers with FXS also meet diagnostic criteria for ASD (Roberts et al., 2020). Additionally, ASIBs are often impacted by the broader autism phenotype, in which they display higher rates of subclinical ASD symptoms than observed in the general population (e.g., Ozonoff et al., 2014). We aimed to examine differences in neural responses to social and non-social stimuli in heterogeneous groups of participants impacted by ASD, including children with ASD, children with FXS, and unaffected ASIBs. Participants included children with ASD (N = 36, 35 males, age M = 5.6 years), children with FXS (N = 19, 13 males, age M = 6.2 years), and non-ASD younger siblings of children with ASD (N = 23, 16 males, age M = 5.5 years). A group of children with typical development were also included (N = 28, 23 males, age M = 5.2 years). Event-related potentials (ERPs) were measured in response to photographs of upright and inverted faces and houses. A behavioral support protocol was utilized to promote successful data collection (Guy, Black, et al., 2021). The P1, indicative of stimulus orienting, and N170, reflecting specialized face processing, ERP components were examined. There was a difference in the amount of useable data collected across groups: ASD (trials M = 159), FXS (trials M = 127), ASIB (trials M = 221), TD (trials M = 206). As presented in Figure 1, there was a main effect of group on P1 amplitude, F(3, 6696) = 37.00, p < .01, η2 = .02. As presented in Figure 2, there were main effects of stimulus type, F(1, 159) = 6.26, p = .01, η2 = .03, and group, F(3, 6675) = 90.35, p < .01, η2 = .04, on N170 amplitude. There were no differences between the groups in the latency of the P1 or N170 ERP responses. However, the group average N170 ERP for the ASD participants appeared to occur later than for the other three groups. These results show distinct differences between the ERP responses of the children with familial ASD (ASD, ASIB) compared to the FXS children. The similarity of the ASD and ASIB responses suggest a common genetic or environmental origin of the reduced response to faces. The FXS children have a high incidence of ASD outcomes, but demonstrate a unique pattern of responses in this study. These results suggest increased activation during face processing in the FXS participants, both in sensory orienting (P1) and face processing (N170).