Subretinal fibrosis is a vision-threatening condition characterized by the formation of fibrous scar tissue beneath the retina, often as a consequence of neovascular age-related macular degeneration (nAMD) or other exudative retinal diseases. The fibrosis results from chronic inflammation, persistent leakage, and proliferation of fibroblasts and myofibroblasts in response to choroidal neovascularization. Currently, there is no direct anti-fibrotic therapy approved for subretinal fibrosis. Standard treatment focuses on controlling the underlying neovascular activity using anti-vascular endothelial growth factor (anti-VEGF) agents, such as ranibizumab, aflibercept, or brolucizumab, which can help reduce exudation and delay or limit fibrotic progression. However, these therapies do not reverse existing fibrosis, and patients with established subretinal fibrotic lesions often continue to experience irreversible visual decline. Emerging strategies under investigation include the use of anti-inflammatory agents, anti-fibrotic molecules targeting TGF-β or CTGF pathways, and gene therapy aimed at modulating the fibrotic response. These approaches aim to supplement anti-VEGF therapy by targeting the scarring process more directly, offering hope for improved long-term outcomes in affected patients.