PLXNB2 and glioblastoma: These data may not be in conflict with one another, as GBM cells may be able to achieve optimal expression levels of Plexin-B2 protein required for desired biomechanical plasticity through feedback regulatory mechanisms onto the endogenous PLXNB2 promoter or by regulation of mRNA translation, which contrasts with our current experimental paradigm of forced lentiviral overexpression of Plexin-B2 cDNA under a constitute promoter without regulatory sequences in 5′ and 3′UTRs.