Further, preclinical data suggest that genetic links (activation of oncogenes such as EGFR, RAS or MET, and inactivation of tumor suppressor genes such as p53 or PTEN) directly induce the expression of genes controlling hemostasis (such as TF gene), which can extend systemically hypercoagulability and cancer progression [12–19]. The gene discussed is EGFR; the disease is neoplasm.