Recent studies have shown that sunitinib-mediated VEGFR2 silencing participates in regulating pluripotency in embryonic stem cells [38] and triple-negative breast cancer [39], and that a stable mesothelioma cell line derived from a patient over-expressing VEGFR2 and c-MYC had stem-like traits [15]. The gene discussed is MYC; the disease is triple-negative breast carcinoma.