Therefore, our data not only suggests a role for HB-EGF in ovarian tumor growth, but also identifies macrophages as a likely source of this growth factor and MMP-9 as a mechanism for controlling HB-EGF bioavailability, providing a clinical rationale for targeting both HB-EGF and MMP-9 in the tumor microenvironment. The gene discussed is MMP9; the disease is neoplasm.