We observed that the RhoA distribution changed: in untreated GBM cells lines, RhoA-associated fluorescence was located in the proximity of the plasma membrane, while in treated cells, RhoA-associated fluorescence was located in the perinuclear region and widespread in the cytosol, suggesting that iPA induced a delocalization of RhoA from the cell membrane to the cytoplasm and this effect determined a disruption of skeleton actin stress fibers. This evidence concerns the gene RHOA and glioblastoma.