The mutant forms of ANG also have impaired neuroprotective ability 40, and are proposed to act through impaired inhibition of apoptosis via the phosphatidylinositol 3-kinase/protein kinase B (PI3K–AKT) signalling pathway 41, a mechanism also implicated in SOD1-related ALS 42. The gene discussed is AKT1; the disease is amyotrophic lateral sclerosis.