C5 and amyotrophic lateral sclerosis: The etiology of ALS is unknown, but neuroinflammation is implicated as a possible driver of disease progression, and complement activation may play a role.1 Activation of the complement cascade has been demonstrated in biofluids and tissue samples from patients with ALS.2,3,4 Additionally, preclinical studies in ALS animal models have shown delayed onset of motor symptoms, improved motor function, and improved survival with C5-mediated complement inhibition.5,6