Our hypothesis states that immunoliposomes may induce the reversion of the immunosuppressive tumor microenvironment by blocking the PD-1/PD-L1 interaction and contributing to increase cell internalization of Dox and thereby, drug cytotoxicity and immunogenic cell death activity, a dual mechanism able to promote an enhancement of the antitumor response. The gene discussed is PDCD1; the disease is neoplasm.