Having established that the deletion of PTPN2 in T cells is sufficient to promote STAT-1 signaling and CD3ε T cell infiltration and repress AT3-OVA tumor growth, we next determined if administering the inhibitor might be accompanied by further increases in intratumoral STAT-1 signaling and T cell infiltration (Fig. 7e). The gene discussed is CD3E; the disease is neoplasm.