To test this hypothesis Htr1acR/cR animals were crossed to Emx1-Cre transgenic mice (Emx1Cre; Iwasato et al., 2000) in order to increase Htr1a expression selectively in principal cortical neurons and examine whether expression of Htr1a under control of its endogenous promoter in this cell-type was sufficient to modulate anxiety behavior. The gene discussed is HTR1A; the disease is Anxiety.