A previous study reported that IL-6 induces VEGF and CCL2 expression in vascular endothelial cells leading to the development of CNV.[51] Additionally, in human AMD, high levels of IL-6 in the blood samples from patients with nAMD correlated with disease progression.[52] TGFβ2 promotes IL-6 production in RPE cells.[53] Sato et al found that IL-6 plays a pivotal role in the development of subretinal fibrosis.[54] Blockade of IL-6 receptor significantly decreased subretinal fibrosis and the JAK1–ERK pathway could be involved in the regulation of subretinal scar formation.[54]. This evidence concerns the gene JAK1 and age-related macular degeneration.