Using inflammatory PMN isolated from WT and Sparc−/− mice, we evaluated whether tumor cells, according to their ability to promote MDSC differentiation (SN25ASP > SN25A), can inhibit such PMN function and whether PMN from SPARC-competent and -deficient mice are differently susceptible to tumor induced re-education and therefore capable of different cytostatic activity on tumor cells. The gene discussed is SPARC; the disease is neoplasm.