This unique ability to counteract Tregs and correct immune tolerance in a TGFβ-enriched tumor immune microenvironment enables a-CTLA4-TGFβRII to be significantly more effective in activating antitumor immunity and inhibiting tumor progression compared with a CTLA-4 antibody, a PD-1 antibody, or even the combination of both mAbs. The gene discussed is CTLA4; the disease is neoplasm.