Hence, we hypothesized that the transfer of NEAT1 via PCa‐derived exosomes might alter the osteogenic differentiation of MSCs by regulating RUNX2 expression through miR‐205‐5p via the SFPQ/PTBP2 axis and designed the current study aiming to validate our hypothesis and uncover a novel therapeutic target for PCa. The gene discussed is NEAT1; the disease is posterior cortical atrophy.