The molecule serotonin (5-HT) is a key factor in the brain involved in feelings of reward and it interacts with specific transporters at the synapses of neurons in the brain. These transporters, termed SERTs, are known to influence the signaling activities of serotonin and have been pharmacologically targeted by antidepressants and psychostimulants in the treatment of mental illnesses. Altered SERT expression and function in the brain is theorized to contribute to multiple neuropsychiatric disorders, including anxiety, obsessive compulsive disorder, depression, and suicide. The majority of studies that explore the contribution of SERT to mental illness have focused on disorders of adult onset. However, increasing evidence demonstrates that 5-HT signaling in the developing brain is critical to establish normal connectivity and behavior. A key example is autism spectrum disorders (ASD), which has been extensively linked to abnormal 5-HT regulation in scientific research for the past 50 years. In this study, researchers have identified rare variations in the SERT gene sequence in individuals with ASD who exhibit observable differences in serotonin transport levels. With this information, researchers have developed a novel, mouse model that exhibits specific expression patterns of a SERT gene variant. As SERT is responsible for inactivating serotonin in the brain, researchers hypothesize that altered availability of serotonin contributes to aspects of phenotypic symptoms observed in ASD.