Given the prominent role of Tregs in suppressing anti-tumor immunity in NSCLC and other tumor types (20, 26–28), we hypothesized that the efficacy of BEMPEG and anti-CTLA-4 in controlling micrometastatic NSCLC might result from overcoming Treg-mediated immune suppression with anti-CTLA-4 (37) and selectively stimulating clonal expansion of effector lymphocytes but not Tregs with BEMPEG (24). The gene discussed is CTLA4; the disease is neoplasm.