As summarized in Figure 8, our data support that YAP/TAZ are critical regulators in mediating HTM cellular responses to the stiffened ECM and elevated TGFβ2 in POAG involving both ERK and ROCK signaling with likely crosstalk; we propose that increased YAP/TAZ nuclear retention may drive further HTM tissue stiffening to exacerbate disease pathology conditions. Here, TGFB2 is linked to open-angle glaucoma.