SPOP also acts as a negative regulator of PCa cell proliferation through the activation of both phosphatidylinositol 3-kinase (PI3K)-AKT serine/threonine kinase (AKT)-mammalian target of rapamycin (mTOR) and AR signaling [36], with SPOP-mutated PCa cells being resistant to bromodomain and extra-terminal motif (BET) inhibitors [37]. Here, AKT1 is linked to posterior cortical atrophy.