This hypothesis was confirmed when we silenced endogenous CORT levels in AI-PCa cells which resulted in a significant increase in proliferation rate in these cells, and in the modulation of the expression/levels of critical genes and oncogenic signaling pathways, including the reduction in the expression of different cell cycle inhibitors (e.g., CDK2, CDKN1A, CDKN1B, and/or CDKND). The gene discussed is CDKN1A; the disease is posterior cortical atrophy.