The molecular basis with which we acquire and maintain sociality has been still unknown. Autism spectrum disorder (ASD) is defined by social communication deficits, indicating the molecular basis of sociality should be damaged in this condition. Many genes associated with ASD encode proteins involved in synapse formation or maintenance, especially synaptic adhesion molecules (SAMs). On the other hand, sex hormones may be involved in ASD onset, but its molecular basis remains uncertain. Here, we show a novel interaction between sex hormones and SAMs. We focused on Octodon Degus as a model animal due to their highly organized sociality. Degus are medium-sized diurnal rodents, and communicate with each other by using more than 20 vocal repertoires. We investigated amino-acid sequences of several SAMs expressed in degus brains and compared with those of humans. Interestingly, a particular SAM of degus shared more than 90% homology with human sequence. We analyzed the binding of the SAM pairs and revealed that a sex hormone disrupted their binding. We also found that one of these SAMs directly binds to the sex hormone. Therefore, we show a possible molecular mechanism of sex hormones affecting ASD and sociality formation.