Recent studies including ours show that active Wnt/β-catenin signaling inhibits fibrosis-associated proteins in the TM and that the POAG-associated Wnt antagonist sFRP1 increases ECM deposition, TM cell stiffness,46 and IOP.10,19 We also have shown that the Wnt/β-catenin signaling pathway and the TGFβ/Smad signaling pathway, another important pro-POAG pathway, cross-inhibit each other in the TM,22 suggesting another way by which Wnt/β-catenin signaling regulates TM homeostasis and IOP. Here, TGFB1 is linked to open-angle glaucoma.