TP53 and glioblastoma: Finally, cell viability assays performed in U87-MG and IR R-1 clones with Rho inhibition associated with or independent of p53 knockdown showed that IR R-1 clones maintained their resistance to IR even in the setting of p53 knockdown when compared to U87-MG cells; however, Rho pathway inhibition with C3 toxin reversed the IR-R-1 clones’ resistance to IR, and this effect was abolished by p53 knockdown (Fig. 8H), again confirming the interdependence between the Rho and p53 pathways in mediating glioblastoma resistance traits.