Using human retinal endothelial cells, one study found that hyperglycemia or euglycemia treatment induces TLR2 and TLR4 expression and subsequent NF-κB p65 activation—thus, producing increased levels of IL-8, IL-1β, TNF-α, MCP-1/CCL2, and enhanced monocyte adhesion to human retinal endothelial cells—while TLR-4/2 inhibition attenuates these phenotypes [345]. The gene discussed is CCL2; the disease is Hyperglycemia.