The involvement of inflammation in the pathophysiology of PSD was initially based on an inflammatory hypothesis (3, 4) in which acute stroke induces a wide spectrum of central and peripheral immune-inflammatory responses, accompanied by upregulation of various pro-inflammatory cytokines (interleukin [IL]-1β, tumor necrosis factor [TNF]-α, interferon [IFN]-γ and IL-6, for instance) (5), subsequently resulting in increased expression of the gene encoding enzyme indoleamine 2,3-dioxygenase (IDO) 1 that triggers the depletion of serotonin, a unanimously identified feature of depression (6). Here, IL1B is linked to depressive symptom measurement.