Also in a pancreatic cancer model, the use of HSV-1 expressing murine OX40L ((OV-mOX40L) triggered an OX40-OX40L signaling pathway-mediated response that also reprogrammed macrophages and neutrophils to an anti-tumor state, enhanced the anti-tumor response of T cells, and significantly prolonged the survival time of mice [107]. The gene discussed is TNFRSF4; the disease is neoplasm.