Studies have since demonstrated that Rac1 is activated in choroidal endothelial cells by several AMD-associated stresses, tumor necrosis factor alpha (TNFα) [26], an example of an inflammatory cytokine; vascular endothelial growth factor (VEGF) [27,28,29,30,31,32] or C-C motif chemokine 11 (CCL11) [30], angiogenic stimuli; reactive oxygen species (ROS) [26]; and 7-ketocholesterol (7KC) [29,33], an oxidized cholesterol that accumulates in human Bruch’s membrane (Figure 1). This evidence concerns the gene RAC1 and age-related macular degeneration.