The explanations for this paradoxical up-regulation of SGK1 in response to the ketamine treatment could lie in at least two key points: first, the neuronal model of glutamatergic activation differs from the canonical assessments of dopaminergic and serotoninergic neurons target for classical anti-depressants; second, it should be borne in mind that the rapid effect of ketamine is accompanied by a controlled dissociative state that could be related to high levels of anxiety-dependent stress probably with increase glucocorticoid release. The gene discussed is SGK1; the disease is Anxiety.