In conclusion, the presently identified pathway of CD73 activity as a source of extracellular adenosine sustaining the activation of A2AR to control amygdala LTP and fear memory prompts consideration of the manipulation of CD73 as a new possibility to pharmacologically correct different behavioral responses that are proposed to be dependent on the function of amygdala A2AR, in particular, abnormal fear memory processing [5], social interactions [8], anxiety [6] or binge eating [65]. The gene discussed is ADORA2A; the disease is Anxiety.