Therefore, inhibition of this pathway using anti-IGF-IR antibodies or expression of truncated IGF-I receptors (via recombinant adenovirus technique) that function as a dominant-negative form of IGF-IR has been examined in the preclinical setting and shown to inhibit the growth of xenograft tumors by up-regulating stressor induced apoptosis, blocking IGF-I and IGF-II induced activation of AKT-1, as well as sensitizing tumor cells to chemotherapy (Maloney et al., 2003; Min et al., 2003; Hezel et al., 2006). This evidence concerns the gene IGF1R and neoplasm.