Prior studies examining the effect of autocrine HB-EGF on ovarian cancer cells found that HB-EGF increased adhesion, invasion, and VEGF production in vitro, and that the HB-EGF inhibitor CRM197 abrogated metastasis in xenograft models [13], suggesting that therapeutically targeting HB-EGF or its receptor EGFR could slow tumor growth. The gene discussed is VEGFA; the disease is neoplasm.