To begin to determine differences in pathological events that may account for the earlier symptom onset, we also focused on glial activation, as increases in CSF IL6 were unique to ALS patients vs. healthy or disease controls [5], and in the clinical trial treating ALS patients with the IL6R inhibitor tocilizumab (TCZ), only individuals inheriting the Ala358 variant and treated with TCZ showed decreases in CSF c-reactive protein (CRP), a marker of inflammation [8]. The gene discussed is IL6; the disease is amyotrophic lateral sclerosis.