While most anti-angiogenesis candidates have targeted the prototypical vascular endothelial growth factor variant A (VEGFA) to normalize tumor vasculature and thereby enhance tumor exposure to cytotoxic agents, upregulation of the related placental growth factor (PlGF) presents a potential mechanism of resistance to VEGFA blockade in addition to being an independent risk factor for cancer progression [4–8]. This evidence concerns the gene VEGFA and neoplasm.