Our study demonstrates the following findings (Fig. 8b): (1) IGF-1R blockade by treatment with anti-IGF-1R monoclonal antibody cixutumumab reprogrammes cancer cells to activate STAT3, leading to transcriptional upregulation of IGF-2; (2) IGF-2 acts as a chemoattractant to monocytes and fibroblasts via utilization of IGF-2R on stromal cells; and (3) infiltrated stromal cells produce various proangiogenic cytokines, most notably CXCL8, which act as chemoattractants to VE cells, resulting in tumour angiogenesis and thus facilitating cancer metastasis. The gene discussed is CXCL8; the disease is cancer.