Based on the above-mentioned data, it might be hypothesized that under pathological conditions (e.g., major depressive disorder, addiction, and suicidal behavior), the balance between 5-HT2A and TrkB becomes shifted toward increased levels of 5-HT2A–TrkB heteroreceptor complexes, with a subsequent loss of TrkB function. This evidence concerns the gene HTR2A and major depressive disorder.