CTLA4 and neoplasm: We reasoned that this locally active modification of the tumor microenvironment presented opportunities to amplify pre-existing or nascent anti-tumor immune responses in environments that monoclonal antibodies cannot penetrate, and/or without the risk of systemic side effects, as have been seen with “checkpoint inhibitor” strategies with systemic administration of monoclonal antibodies against CTLA4, PD1/PDL1, or combinations thereof.31, 32