As we describe above, since 2009, Zlokovic and colleagues have provided evidence that APC or APC analogs lacking anticoagulant activity slowed disease progression and extended survival of SOD1 mice with ALS-like characteristics, an effect that required PAR1 and PAR3 and that led to decreased expression of mutant SOD1 [109]. The gene discussed is APC; the disease is amyotrophic lateral sclerosis.