Our results indicate that miRNA-302a suppressed the proliferation and tumorigenicity of PCa cells through the AKT-GSK3β-cyclin D1 and the AKT-p27Kip1 pathway, and by directly binding the 3 ́UTR of AKT. Furthermore, the expression of PI3K, which is principal upstream effector of AKT and has also proven important in PCa development, were not affected by miRNA-302. The gene discussed is CCND1; the disease is posterior cortical atrophy.