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. This evidence concerns the gene LTBP2 and Fuchs endothelial corneal dystrophy.