In support of this idea is the fact that CORT silencing in AI-PCa cells induced significant changes in the expression levels of key cell cycle/proliferation markers and SSTR-subtypes, such as modulation of CDK2, CDKN1A, CDKN1B, CDKND, SSTR1, SSTR2, and/or SSTR5. The gene discussed is CDKN1A; the disease is posterior cortical atrophy.