AH levels of TGF-β2 (1.94 to 3.46 ng/mL) in patients with primary open-angle glaucoma (POAG) were shown to be significantly higher than those in non-glaucoma patients (0.41 to 2.24 ng/mL) [6,7], suggesting that TGF-β2 indeed induces excessive deposits of ECM within the TM, leading to elevation in POAG [8,9,10] as the glaucomatous TM phenotype [11]. The gene discussed is TGFB2; the disease is open-angle glaucoma.