Our study is based on the strong, specific pre-clinical rationale that chemotherapy, while beneficial, also instigates a paracrine inflammatory loop involving the tumor and stroma, whereby cytotoxic stress induces endothelial cell secretion of TNF-α, which promotes cancer-cell secretion of CXCL1/2 and the recruitment of CXCR2-expression myeloid-derived suppressor cells (MDSCs). The gene discussed is TNF; the disease is neoplasm.