MYOC (myocilin) is a secreted glycoprotein that regulates multiple signaling pathways controlling cell adhesion, cytoskeleton organization, and cell migration through interactions with Wnt signaling and fibronectin. It modulates stress fiber assembly and focal contact formation while negatively regulating cell-matrix adhesion via Rho protein signaling. MYOC plays roles in bone formation through mitogen-activated protein kinase signaling, peripheral nerve myelination via ERBB2/ERBB3 signaling, and potentially regulates fluid outflow in the trabecular meshwork. MYOC mutations are primarily associated with primary open-angle glaucoma (POAG) and juvenile-onset glaucoma. Mutations account for 3-4% of POAG cases worldwide 1, with penetrance varying significantly by mutation site (10.3%-100%) and ethnicity, ranging from 54-71% in POAG cases 2. Pathogenic variants are predominantly rare missense mutations in the conserved olfactomedin domain, while truncation variants show limited evidence for causation except p.Gln368Ter 3. Penetrance increases with age and is higher in Asian populations 2. A polygenic risk score incorporating MYOC variants enables risk stratification and predicts disease progression 4. However, MYOC promoter polymorphisms and variants show no significant association with steroid-induced ocular hypertension 56.