Social communication impairments have been a defining feature of autism spectrum disorder (ASD) since Leo Kanner’s seminal description of 11 children with idiosyncratic social behaviors. In the 75 years since Kanner’s pivotal article, ASD research has focused on understanding and ameliorating the social communication and social cognitive impairments that are a defining feature of the disorder. Recently, however, the social motivation hypothesis of autism has been proposed as a novel account of the causal mechanisms of social impairments in ASD. This framework suggests that certain individuals with ASD are less motivated to interact with other people and derive less pleasure from social interactions. This account of ASD was initially proposed by Dawson and colleagues in 2005 to describe impaired electrophysiological responses to faces and the potential developmental outcomes of such impairments on the emergence of face expertise in ASD. Chevalier et al expanded the description of this framework in 2012 by considering the behavioral, neurobiological, and evolutionary features of the social motivation hypothesis of autism and suggested brain systems (orbitofrontal–striatal–amygdala neural circuitry) that are likely to account for social motivational impairments in ASD.