St. Pourcain et al., in the third autism spectrum disorder-related paper in this issue (12), take a complementary approach to clarifying the phenotypic spectrum of autism spectrum disorder risk genes. In 2009, Wang et al. (13) reported a genome-wide association study of autism spectrum disorders that found, and replicated in two independent samples, a signal from a set of single-nucleotide polymorphisms (SNPs) between two cadherin genes on chromosome 5, the most significant of which was rs4307059. St. Pourcain and colleagues examined variation in this SNP in 7,313 members of the population-based Avon Longitudinal Study of Parents and Children cohort, looking specifically at 29 measures related to social communication assessed between the ages of 3 and 12. Of the 29 traits examined, two—stereotyped conversation and pragmatic aspects of communication, both assessed at age 9—were significant after correction for multiple testing. More interesting, when the authors combined these traits into an autism spectrum disorder-like phenotypic profile, the association with rs4307059 substantially strengthened with communicative, cognitive, and social-interactive traits playing a particularly strong role in the association. This is an impressive report from a large representative sample, utilizing creative but rigorous statistical methods. Most importantly, the study shows that a genetic variant initially detected in individuals with clinically diagnosed autism spectrum disorders has an impact on functioning in the general population. Again, genes do not seem to respect our diagnostic boundaries. Also noteworthy is that the effect of this variant (which was very small—no more than 0.3% of any individual trait) was more robustly detected by a spectrum of phenotypes than by any one measure alone.