The combination of intraperitoneally (i.p.)administered mAb antagonizing CTLA-4 signaling (aCTLA-4 mAb) with i.t. GSNO treatment was evaluated for its potential to unleash the functions of activated and mature DCs that appear to be restrained by CTLA-4 expressing tolerogenic DCs, macrophages, and MDSCs induced by GSNO treatment (Figs. 1, 2) using a dual B16F10-OVA mouse tumor model to reveal direct as well as abscopal therapeutic effects (Fig. 3a). This evidence concerns the gene CTLA4 and neoplasm.