In PCa, JUNB, Fos, and JUND are associated with combinations of signaling events, including c-JUN amino-terminal kinase (JNKs), extracellular signal-regulated kinases (ERKs), and other regulatory pathways, like PI3K and the p38 family of kinases, which directly activate the transcription of Jun and Fos and are responsible for activating AP-1 [114]. Here, JUN is linked to posterior cortical atrophy.