Scientific rationale for further examining the role of vandetanib in the management of patients with ER+ve/HER2–ve metastatic breast cancer is supported by cell line experiments demonstrating that breast cancer cell growth (along with key downstream kinase activity and ER cross-talk) is significantly inhibited by vandetanib, particularly in the setting of endocrine-resistant compared to endocrine responsive cells [5]. The gene discussed is ERBB2; the disease is breast cancer.