Taking advantage of the ALS mice overexpressing TGFB1 in astrocytes and of the ALS mice with the astrocyte-specific deletion of TGFB1, they determined that astrocyte-derived TGFB1 accelerates disease progression in ALS mice, preventing neuroprotective responses mediated by the microglia and T cells [12]. This evidence concerns the gene TGFB1 and amyotrophic lateral sclerosis.