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Filtration surgery is now the most effective and popular surgical procedure for glaucoma, and anti-proliferative agents such as Mitomycin C or 5-fluorouracil are generally concomitantly used for improving success. However, filtration surgery is not perfect. Filtering bleb often fails to reduce intraocular pressure by fibrosis or other reasons. Patients never are free from the possibility of bleb-related complications. Seet et al. (2026) offer a new approach for preventing fibrosis of filtering bleb by targeting SPARC (secreted protein, acidic and rich in cysteine) in this paper. SPARC is known to modulate cell to extracellular matrix (ECM) interaction, and its role has been reported in other fields such as skin, lung, and others. The authors performed in vitro and in vivo studies using the SPARC deficiency mouse. SPARC plays a key role in formations of collage type I and fibronectin against TGF-beta-2 loading. SPARC also reduces MMP-2 activity that may inhibit tissue construction. These results indicate that key proteins involving in cell-ECM interaction for scarring or fibrosis are regulated by SPARC. Indeed, their experiments employing SPARC deficiency mouse eyes with filtration surgery showed that filtering blebs of the SPARC deficiency mouse had a longer survival period than that of the wild mouse. These exciting results provide the promise for development of a new generation of filtering surgery. However, one wonders if regulation of SPARC may reduce the possibility of the bleb-related complications such as endophthalmitis.