14, 15 We previously demonstrated that L-plastin is upregulated by both oestrogen and androgen exposure in a hormone-sensitive PCa model and is associated with a malignant state in prostatic epithelial cells.16 Moreover, we recently noted that androgen-insensitive PCa cells (LNCaP-AI and PC-3 cells) overexpress L-plastin, suggesting that other non-steroid-dependent factors may promote expression of the protein. This evidence concerns the gene LCP1 and posterior cortical atrophy.