Based on prior evidence that pharmacological blockade (Vinkers et al., 2010; Sarkar et al., 2014) or genetic loss of function of the Gi-coupled 5-HT1A receptor results in enhanced anxiety- and despair-like behavior (Gross et al., 2002; Richardson-Jones et al., 2010, 2011), a working hypothesis would suggest the possibility that enhancing Gi signaling in CaMKIIα-positive forebrain excitatory neurons during the postnatal window might evoke a decline in anxiety- and despair-like behaviors in adulthood. This evidence concerns the gene GNAI1 and Anxiety.