PRKCH encodes protein kinase C eta, a calcium-independent, phospholipid- and diacylglycerol-dependent serine/threonine kinase with diverse cellular functions. In keratinocytes, PRKCH promotes differentiation by binding and activating FYN kinase, which inhibits EGFR signaling and induces G1 cell cycle arrest through CDK2 inhibition and RB1 dephosphorylation. The enzyme regulates epithelial tight junction integrity by phosphorylating occludin on threonine residues, essential for junction assembly and maintenance. In glioblastoma cells, PRKCH promotes proliferation via mTOR and PI3K/AKT pathway activation while preventing apoptosis by inhibiting caspase-9 activation 1. PRKCH also functions in B cell receptor signaling, foam cell formation, and protects cancer cells from DNA damage-induced apoptosis by modulating NF-κB signaling. Clinically, PRKCH polymorphisms associate with ischemic stroke risk, particularly lacunar infarction, in Asian populations. The 1425G/A SNP shows consistent association with stroke (OR=1.34-1.37 across studies), with the A-allele conferring increased risk 23. This polymorphism also associates with sudden sensorineural hearing loss, suggesting vascular pathogenesis 4. Additionally, PRKCH variants influence antihypertensive efficacy of telmisartan 5, and the gene shows association with rheumatoid arthritis susceptibility in Japanese populations 6. PRKCH represents both a biomarker for stroke risk and a potential therapeutic target in glioma and other malignancies.