The major mechanisms of action of ketamine (and its metabolites) in depression are (1) its antagonism of the NMDA subtype of glutamate receptor, (2) its inhibition of the phosphorylation of the eukaryotic elongation factor 2 (eEF2, also called CaMKIII) thus resulting in increased synaptic protein synthesis, (3) its action via the mammalian target of rapamycin (mTOR) dependent synapse formation, (4) its inhibition of the nicotinic acetyl choline receptor (NAR), and (5) its suppression of the glycogen synthase kinase 3 (GSK-3) [14, 15]. This evidence concerns the gene MTOR and depressive symptom measurement.