Several studies have indicated that AKR1C3 overexpression increases with PCa progression through the mechanisms underlying the key steroidogenic enzyme AKR1C3, which possesses 17β-hydroxysteroid dehydrogenase type 5 (17β-HSD5) activity, and PGF synthesis enzyme [13,16,17]. Here, AKR1C3 is linked to posterior cortical atrophy.