These lymphomas were shown to be able to exert their immunosuppressive function by binding of B7.1 and thus reducing CD28 activation on tumor-infiltrating/immunosurveillance T-cells; furthermore—as in T-cell lymphomas—CTLA4 can enhance proliferation via the STAT3 pathway, which is an important driver also in B-cell lymphomas (84). This evidence concerns the gene CD28 and T-cell non-Hodgkin lymphoma.