Thanks to growing insights into the suppressive mechanism of the tumor microenvironment, possible ways to block tumor escape are currently under investigation, including the delivery at the site of the tumor of immune stimulatory molecules (e.g., OX40 ligand and IL-23 [3]), blockade of inhibitory cytokines (e.g., TGF-β receptor II to capture TGF-β [4]), as well as immune checkpoint blockade (e.g., PD-1 or CTLA-4 [5,6,7]). Here, CTLA4 is linked to neoplasm.