Interestingly, recent findings suggest that treatment of ALS mice models with unmodified human bone marrow CD34+ (hBM34+) cells accelerates BSCB repair, leading to differentiation into endothelial cells, reduced astrogliosis and microgliosis, and improved perivascular integration, ultimately promoting survival of motor neurons141; likewise, treatment with pericytes improves overall survival in SOD1 mutant ALS mice142. Here, SOD1 is linked to amyotrophic lateral sclerosis.