Despite these notable differences, which may be largely attributed to epitope specificity, both agonistic and antagonistic types are known to cause the degradation of IGF-1R, which has been advocated as the primary mechanism for the observed activities of various anti-IGF-1R antibodies in inhibiting anchorage-independent growth, motility, and invasion of cancer cells in vitro [39], [59], [60], as well as in reducing the colonization of xenograft tumors in metastatic animal models [61]. The gene discussed is IGF1R; the disease is cancer.