Specifically, the characterization of the acute post-translational upregulation of EphB4 in response to autocrine IGF-II has been demonstrated by our observation that deprivation of the autocrine IGF-II signal in cultured cancer cells using a neutralizing anti-IGF-II antibody caused a marked and rapid decrease in EphB4 total protein levels (5). The gene discussed is EPHB4; the disease is cancer.