In conclusion, using our bioengineered tissue-mimetic ECM hydrogel system, we demonstrated that nuclear YAP/TAZ is upregulated in response to simulated glaucomatous conditions (i.e., TGFβ2 induction and stiffened ECM), and that YAP/TAZ activation induces HTM cell contractility and ECM remodeling, which together may increase HTM stiffness in POAG. The gene discussed is WWTR1; the disease is open-angle glaucoma.