These microscopic and submicroscopic CNVs are presumed to have a major and sometimes causal impact on risk for ASD. In contrast, common variants rarely have such an impact on risk for any disorder, especially one like ASD that is known to diminish reproductive success. Nonetheless, even if a common variant has only a small impact on individual risk, its population attributable risk could be substantial because it is carried by many individuals. To date, studies identifying common variants affecting ASD risk have met with limited success. In addition to candidate-gene association studies, in which some genes garner supporting evidence (19), genome-wide association (GWA) studies have highlighted two ASD risk loci: 5p14.1, between the neuronal cadherin loci CDH9 and CDH10 (20), and 5p15.2, between the semaphorin (SEMA5A) and bitter taste receptor (TAS2R1) genes (21).
