The mechanism of arsenic-induced angiogenesis involves the excessive formation of ROS, which in turn activates one of the frequently deregulated pathways in human cancers, involving the Akt signaling pathway, the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway, and the increased expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF) (Liu et al. 2011; Gao et al. 2023). The gene discussed is VEGFA; the disease is cancer.