One possible mechanism for this process was proposed by Mo et al. [95], who showed that the expression of long noncoding RNA nuclear-enriched abundant transcript 1 (lncRNA-NEAT1) is enhanced in hBMSC by PCa-derived exosomes and contributes to osteogenic differentiation of hBMSC via miR-205-5p regulation. The gene discussed is NEAT1; the disease is posterior cortical atrophy.