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. The gene discussed is C3; the disease is glioblastoma.