Our results further support the potential role of CCL-2 and IL-2 in negative regulation of pancreatic tumor progression through stimulation of innate immune response given the regression in tumor volume within TPV/∆66R/mIL-2-treated subjects and statically significant regression in tumor volume in TPV/∆66R/mCCL-2-treated subjects compared to vehicle control immunocompromised subjects. The gene discussed is IL2; the disease is neoplasm.