It thus may be of interest to understand and model how to optimize NF-κB stimulation via a combination of agonists (e.g. OX40 and 4-1BB) and antagonists (e.g. CTLA-4 and PD-1), and how the responsivity of the T cells to these therapies may change under conditions of tumor-mediated immunoediting, as tumors are known to secrete factors that may inhibit TCR-mediated NF-κB activation (and, potentially, OX40- and 4-1BB-mediated NF-κB activation). The gene discussed is NFKB1; the disease is neoplasm.