Therefore, the inhibition/deletion of PTP1B and/or PTPN2 in resident/infiltrated T cells in immunogenic tumors would not only facilitate T cell activation, but also, as a consequence of heightened CD8+ T cell IFNγ production in the tumor microenvironment, exacerbate inflammation and promote the further recruitment and activation of T cells to repress tumor growth. The gene discussed is PTPN2; the disease is neoplasm.