For instance, some reports suggest that low concentrations of 2‐AG alleviate anxiety, while high concentrations tend to induce anxiety in both humans and rodents.[9, 34] Systemic knockout of the 2‐AG hydrolase enzyme monoacylglycerol lipase congenitally increased 2‐AG levels in the amygdala, causing CB1R desensitization and compensatory damage to CB1R signaling, resulting in anxiety.[35, 36] Given these complexities, a more detailed investigation of the role of eCB signaling in the BLA‐vHPC circuit in anxiety is necessary. The gene discussed is CNR1; the disease is Anxiety.