Indeed, there are numerous findings regarding the pathophysiology of depression, which may become new drug targets, such as abnormalities in glutamatergic neurotransmission, neuroendocrine theory, inflammation or neurotrophic conception based on the reduced expression of brain-derived neurotrophic factor (BDNF) and/or the failure of its receptor—tyrosine receptor kinase B (TrKB) [24,25,26,27]. The gene discussed is NTRK2; the disease is depressive disorder.