KDR and neoplasm: After activation, multiple pathways have been proposed mediating the action of the generated reactive oxygen species (ROS), such as weakening the integrity of the cell, inducing cell cycle arrest, apoptosis, and autophagy [12], or suppressing angiogenesis by inhibiting the secretion of VEGF, VEGFR2, and KDR/flk-1 in tumors [21], or affecting signaling pathways and transcription factors associated with tumor growth, including the AMPK pathway, the Wnt/β-catenin pathway, nitric oxide signaling, CREBP, NF-κB, and MYC/MAX [22].