While we observed a survival benefit conferred by TH-302 and VEGFR-2 in an orthotopic, transplantable murine model of pancreatic cancer and identified the CCL9/CCR1 axis as responsible for the recruitment of G-MDSCs to the tumor microenvironment posttherapy, we acknowledge that these conclusions are drawn from 1 pancreatic tumor cell line. This evidence concerns the gene CCR1 and neoplasm.