Wet AMD is caused by choroidal neovascularization (CNV) whereby new abnormal blood vessels spread beneath the retina. These vessels may rupture and cause retinal damage. In addition, vascular leakage may cause thickening and oedema of the retina, which is thought to contribute to vision loss. Vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) play a pivotal role in this scenario. VEGF-A and PlGF are members of the VEGF family of angiogenic factors that act as potent mitogenic, chemotactic, and vascular permeability factors for endothelial cells. VEGF acts via two receptor tyrosine kinases—VEGFR-1 and VEGFR-2—which are located on the surface of endothelial cells. PlGF binds only to VEGFR-1, which is also present on the surface of leukocytes. Excessive activation of these receptors by VEGF-A can induce pathological neovascularization and excessive vascular permeability. PlGF can synergize with VEGF-A in these processes, and is also known to promote leukocyte infiltration and vascular inflammation.