In this study we evaluate the impact of a STING agonist, ADU-S100, a synthetic cyclic dinucleotide (CDN) agonist of STING, known to activate all human and mouse STINGs and induce the expression of cytokines and chemokines [18], in combination with radiation, on local tumor control and effector T-cell functionality using the modified Levrat model for esophageal adenocarcinoma (EAC). The gene discussed is STING1; the disease is neoplasm.