According to reports, Disulfiram enhances T-cell anti-tumor immunity by directly activating lymphocyte-specific protein tyrosine kinase (LCK)-mediated TCR signaling.[17] And diflunisal targets HMGB1/CXCL12 heterotrimeric complex and blocks immune cell recruitment.[18] We evaluated the association between disulfidptosis risk model and immune cell abundance. The gene discussed is HMGB1; the disease is neoplasm.