Our results on the tyrosine-specific phosphorylation of TrkB (Tyr706/707 and Tyr816 sites, but not at Tyr515) in the brain areas implicated in depression, caused by prolonged GSB-106 treatment in UCMS-exposed mice, are in line with the data observed on typical antidepressants, which provide TrkB-Tyr816/PLC-γ1 specific effects [18,19]. Here, NTRK2 is linked to depressive disorder.