A study addressing why the IGF-1R pathway silencing through IGF-1R fusion protein IGF-Trap-induced IGF-1/2 bioavailability reduction, which was a promising anticancer strategy in vitro failed in nude mice xenotransplanted with the human triple negative breast cancer MDA-MB-231 cells, found that these cells developed resistance to IGF-targeted therapy by increasing the activation of another receptor tyrosine kinase, fibroblast growth factor receptor 1 (FGFR1) (75). This evidence concerns the gene IGF1 and triple-negative breast carcinoma.