We confirmed that deletion of CD147 in KCs (Fig. 4E) and pharmacological inhibition of glycolysis by 2-DG (Fig. 4F) attenuated the expression of IL-17A-induced proinflammatory molecules, including Cxcl1, Cxcl2, IL-1α, and IL-1β, indicating that increased glycolytic activity aggravated the production of inflammatory factors in KCs. The gene discussed is CXCL1; the disease is dry eye syndrome.