It should be clarified that the mechanism by which ISL exerts its effects in oral tumors is unique, specifically manifested as follows: directly impairing the survival ability of tumor cells by inhibiting the Akt-Wee1-CDK1 signaling pathway and promoting the ubiquitin-mediated degradation of Survivin protein; overcoming cisplatin resistance by downregulating ABCG2/GRP78; and the therapeutic effect of S-ISL. The gene discussed is HSPA5; the disease is neoplasm.