To systematically investigate whether targeted inhibition of NF‐κB or IL‐6 signaling pathways could enhance corneal wound healing under aqueous‐deficient dry eye conditions, LGE‐treated mice were rigorously administered either the NF‐κB inhibitor caffeic acid phenethyl ester (CAPE) or a neutralizing anti‐IL‐6 antibody. The gene discussed is NFKB1; the disease is dry eye syndrome.