Previous studies, including our own, have shown that the deletion of PTPN2 in poorly immunogenic tumors, such as B16F10A or AT3 syngeneic tumors, can significantly enhance T cell recruitment and anti-tumor immunity by promoting IFN-induced STAT-1 Y701 phosphorylation (p-STAT-1) and the expression of chemokines such as CXCL9 and CXCL10 in tumor cells6,10 to facilitate T cell and NK cell recruitment. The gene discussed is CXCL10; the disease is neoplasm.