Furthermore, antibodies against surface molecules (including CD25 [340], CCR4 [341], CTLA-4 [342], OX40 [343], and GITR [344, 345]) exhaust Tregs in various tumor models, and molecules (such as cyclophosphamide [346] and Raf-kinase inhibitor sorafenib [347]) can also preferentially deplete Tregs upon systemic administration. The gene discussed is CTLA4; the disease is neoplasm.