Although the mechanisms by which glucocorticoids lead to glaucoma are not well understood, it has been reported that trabecular meshwork express glucocorticoid receptors and their activation by exogenous steroids, such as dexamethasone, decrease the phagocytic ability of trabecular meshwork cells and downregulate metalloproteinases (i.e., MMP1), thus leading to extracellular matrix deposition, particularly in the juxtacanalicular tissue and along the inner wall endothelium of Schlemm’s canal. The gene discussed is MMP1; the disease is glaucoma.