First, in distinct in vitro models of Ataxia Telangiectasia, ATM-deficient astrocytes were shown to activate their oxidative and ER stress responses, which in turn translated in a senescence-like growth arrest through multiple Extracellular signal-regulated kinases 1/2 (ERK1/2)-dependent mechanisms, as demonstrated by the fact that treatments with the antioxidant N-acetyl-L-cysteine (NAC) not only restored their defective proliferation but also suppressed ERK phosphorylation/activation [111,112,113]. The gene discussed is ATM; the disease is Ataxia-telangiectasia.