We have previously recorded a dose-dependent transactivation of the IGF-1R in several principally different cell types: human breast cancer cells and human aortic smooth muscle cells with constitutive expressions of TF, human monocytes primed to express TF, and porcine aortic endothelial cells transfected with human TF, this after treatment with fully functional FVIIa but not after treatment with an active-site inhibited FVIIa [16, 24]. The gene discussed is TF; the disease is breast carcinoma.