It is striking that the functionality of GABA and 5-HT system in “normal” or “pathological” anxiety in healthy individuals is largely unknown, In case of 5-HT modulation (via 5-HT1A receptor activation or blockade of the 5-HTT) an indirect effect is possibly the most logical explanation, because treatment of anxiety disorders with SSRIs or buspirone takes weeks or even months before anxiolytic activity is seen (acute effects seen after administration of these drugs are even anxiogenic). The gene discussed is HTR1A; the disease is anxiety disorder.