IGF1R and neoplasm: 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.