Abstract: Glaucoma is an optic neuropathy, with pathophysiological changes affecting anterior and posterior tissues of the eye. The trabecular meshwork (TM) in the anterior segment regulates intraocular pressure (IOP), while photoreceptors in the posterior retina convert light into signals that retinal ganglion cells (RGC) transmit to the brain. The TM is a small, fenestrated tissue located in the anterior chamber angle, between the iris and cornea (Figure 1A1). In humans, the majority of aqueous humor fluid drains through the TM into Schlemm’s canal. If the outflow channels become blocked, as in glaucoma, IOP starts to increase, pushing the lens and vitreous back onto the optic disk. Pressure-induced damage to the optic nerve head causes a pro- gressive loss of RGCs and their axons, which leads to irreversible blindness. Surgical or pharmacological management of IOP prevents RGC damage in glau- coma patients. Standard pharmacological therapies either reduce production of aqueous humor fluid, or increase aqueous drainage via the TM or the uveoscleral outflow pathways. Recently, a new class of glaucoma therapies targeting the actin cytoskeleton were approved by the Food and Drug Administration. These are known as the Rho kinase inhibitors, and they act on the Rho/Rho-associated protein kinase signaling pathway to disassemble actin stress fibers in TM and Schlemm’s canal cells (Rao et al., 2017; Lin et al., 2018). While the molecular details are only partially understood, perturbing the actomyosin system can alter cell shape, volume, contractility, and adhesion of cells to extracellular matrix (Tian et al., 2009), which in turn allows greater aqueous outflow and a reduction in IOP. In addition to forming stress fibers, filamentous actin assembles into actin bundles, which are a major component of filopodia, long finger-like projections that emanate from the cell surface, as well as the related cellular protrusions known as tunneling nanotubes (TNTs) .