This approach is expected to minimize systemic drug exposure and promote several anti-tumor immune mechanisms such as (1) activation and maturation of APCs [22], (2) expression of type-I and type-II interferons associated with anti-tumor immunity [23], (3) migration of activated APCs to tumor draining lymph nodes (tDLNs) [24], and (4) activation and recruitment of cytotoxic immune cell subsets to the tumor microenvironment (TME) [8]. The gene discussed is SGCG; the disease is neoplasm.