In castration-resistant neuroendocrine (NE) prostate cancer (PCa), H19 regulates PCa lineage plasticity by driving a bidirectional cell identity of NE phenotype, with H19 overexpression promoting the castration-resistant NE phenotype, while H19 knockdown promotes the luminal type of PCa, which is sensitive to androgen deprivation therapy [52]. Here, H19 is linked to posterior cortical atrophy.