It has been shown, however, that increased leakiness of the in vitro model of the blood-brain barrier, using human brain endothelial cells, was associated with a reduction in the Rac1 (ras-related C3 botulinum toxin substrate 1)/WAVE (Wiskoff-Aldrich Syndrome protein-family verprolin homologous protein)/Arp3 (actin related protein 3) signaling pathway.57 Our findings suggest the presence of echographic signs of brain edema in P5/PELS10 as a raw indicator of blood-brain barrier disruption. This evidence concerns the gene ACTR3 and brain edema.