Since the histological hallmark of aggressive PCa is a poorly differentiated glandular architecture of high Gleason grade and presence of nests of neuroendocrine cells, namely neuroendocrine differentiaton (NED) areas [13, 14], it may be supposed that SNAI2's role in prostate carcinogenesis involves the regulation of stem cell- or NED-associated genes. The gene discussed is SNAI2; the disease is posterior cortical atrophy.