While guttae comprise multiple FECD-associated pathological ECM components, we focused on several key molecules: FN1, which has been well established in previous literature34–36, as well as LTBP2, MATN3, and BGN, which our previous shotgun proteomic analysis identified as upregulated genes in FECD patients37. Here, BGN is linked to Fuchs endothelial corneal dystrophy.