PLXNB1 and posterior cortical atrophy: Intriguingly, we showed that overexpression of PlexinD1 without modulation of Sema ligand levels was sufficient to promote PCa cell proliferation, migration, invasion, ENZ resistance, stemness, and plasticity, which could be possibly attributed to receptor clustering for mimicking ligand binding, a mechanism demonstrated by PlexinB1 previously (Giordano et al, 2002).