The theory of the use of flumazenil in anxiety disorders, such as GAD, postulates that the increase in allopregnanolone in response to acute stress [11,28] and subsequent decrease during chronic stress [29,30,31,32] alters GABAA receptor composition; specifically, an increase in α4βδ GABAA receptors and α4 expression [33,34,35]. The gene discussed is GAD1; the disease is anxiety disorder.