As SD101 has been reported to induce systemic proinflammatory cytokine production, i.e. IL-1β and IP-10 [27], and we indeed confirmed the expression of these, and others, immune mediators in the TME of both treated and untreated contralateral lesions, we investigated whether the systemic anti-tumor effect observed in the contralateral, untreated lesion, was mediated by this “non-specific “ immune response or by the induction/activation of anti-tumor specific cytotoxic T cells by comparing SD101 therapeutic activity in immune-compentent and -deficient mice. The gene discussed is IL1B; the disease is neoplasm.