We argue that adolescents are not necessarily uniquely vulnerable to Trkb. t1 overexpression but are rather more vulnerable to a corticosteroid-induced triggering of neurobiological factors associated with depression-like and habit-based behaviors (in this case, the concomitant elevation of trkB.t1 and reduction in p-ERK42/44 in the vHC). The gene discussed is NTRK2; the disease is depressive symptom measurement.