Growing experience has revealed that IL-17 could downregulate filaggrin and genes associated with cellular adhesion to induce skin barrier disruption (23), thereby eliciting a hypoxia environment and the upregulated expression of vascular endothelial growth factor (VEGF) as part of the pathological basis of psoriasis (24), which is in agreement with the theory that psoriasis could be triggered in the context of reactive oxygen species (ROS) production and a decrease in antioxidant activity (25). The gene discussed is IL17A; the disease is psoriasis.