A major breakthrough in attempts to understand the etiology of glaucoma was the discovery that administration of cortisol to primary cell cultures of human trabecular meshwork cells resulted in pronounced overexpression of a protein, initially designated “trabecular meshwork inducible glucocorticoid response (TIGR) protein,” but more commonly known as “myocilin” (Stone et al., 1997; Clark et al., 2001). This evidence concerns the gene MYOC and glaucoma.