Manipulations of 5HT signaling, either via pharmacologic 5HTT blockade or SLC6A4 knock-out in mouse models, that increase serotonin concentrations during developmentally sensitive periods, are associated with lasting behavioral, neurophysiological, and neuroanatomical changes in animal models (Homberg et al., 2010; Olivier et al., 2011; Simpson et al., 2011) and increased risk for anxiety/depression symptoms in humans (Oberlander et al., 2010; Weikum et al., 2013). The gene discussed is SLC6A4; the disease is depressive symptom measurement.