Infiltration of Treg into tumors is associated with enhanced tumor growth and poor prognosis [1–3] and their therapeutic depletion through antibody-dependent cell-mediated cytotoxicity (ADCC)-proficient antibodies against a Treg-associated molecule CTLA-4 or low-dose cyclophosphamide treatment can improve anti-tumor T-cell responses and overall survival of patients [4, 5]. The gene discussed is CTLA4; the disease is neoplasm.