MAPK pathway components, including c-Jun N-terminal kinases (JNKs) and their canonical target JUN (also known as cJUN), and ER stress signaling, and its downstream effector DNA damage inducible transcript 3, Ddit3 (also known as CCAAT/enhancer binding homologous protein (CHOP)/GADD153), are known to be important pro-apoptotic cascades after glaucoma-relevant injuries [21–36]. Here, JUN is linked to glaucoma.