The details behind the clinical shortcomings of sunitinib in BrCa are not entirely clear but suggested explanations include the growing evidence that BrCa angiogenesis is driven by more than just VEGF, so inhibition of many other proangiogenic kinases might be necessary; the activation of cancer stem cells that overcome tumor remission [10]; and certainly the limitation of administering a higher drug dose due to off-target toxicities such as left ventricular (LV) dysfunction and overt heart failure frequently encountered due to depletion of coronary microvascular pericytes [17]. Here, VEGFA is linked to invasive breast carcinoma.