In mouse models, imiquimod (IMQ)-induced psoriasis-like inflammation was suppressed by either genetically or pharmacologically blocking the expression of glucose transporter 1 (Glut1) or by inhibiting glycolysis by 2-deoxy-D-glucose (2-DG) [9,12], which indicated that highly expressed epidermal Glut1 elevates glycolysis activity and is critical in psoriasis. Here, SLC2A1 is linked to psoriasis.