Importantly, c-Src is known to be over-expressed and/or hyper-activated in a wide variety of human cancers, which is caused by enhanced expression or dysregulation of upstream growth factor receptors and non-receptor tyrosine kinases, such as the epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER2), platelet-derived growth factor receptor (PDGFR), fibroblast growth factor receptor (FGFR), vascular endothelial growth factor receptor (VEGF), integrins, or focal adhesion kinase (FAK) [6–9]. Here, ERBB2 is linked to cancer.