Stat3 activation can occur through the actions of many autocrine and paracrine growth factors (for example, interleukin-6 [IL-6], epidermal growth factor, platelet-derived growth factor, heregulin, vascular endothelial growth factor, and hepatocyte growth factor) and the Src non-receptor tyrosine kinase, leading to the prediction that its phosphorylation in breast cancer would be through these multiple, redundantly acting growth factors [6-8,12,13,18,19,23-25]. Here, STAT3 is linked to breast cancer.