Conventional therapy may induce inflammation and angiogenesis, and metastasis via apoptotic tumor cell‐induced macrophage chemotaxis and proinflammatory cytokines.[21] Angiogenesis is also a critical hallmark of malignant tumor growth.[22] Recent studies suggested that enhanced signaling contributes to VEGF‐independent tumor angiogenesis through a COX‐2/prostaglandin E2 (PGE2) axis.[23] COX‐2/PGE2 inhibition may potentiate VEGF therapies. Here, VEGFA is linked to neoplasm.