Several models of murine glaucoma (e.g. DBA/2J or Col1a1(r/r)) work by physically blocking the meshwork or disrupting extracellular matrix.[7] Since cromakalim works through the conventional outflow pathway, applying cromakalim on these murine models may have been futile in the face of overwhelming physical blockage of the meshwork. Here, COL1A1 is linked to glaucoma.