On the other hand, YKL-40 expression is activated via stimulation of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and interferon-γ, which are released from ischemic penumbra after stroke and further significantly involved in the progression of neuronal necrosis and blood-brain barrier disruption [20, 21]. This evidence concerns the gene IL6 and stroke disorder.