As discussed above and by the signature and biomarker network analyses, SCA pathophysiology at steady state appears to be controlled by Th1 and Th17 cytokines (IL-12, IFN-γ, IL-1β, and IL-17), with IL-8, IL-10, and IP-10 as general biomarkers and MIP-1β and RANTES making a difference in SCA patients with high death risk. The gene discussed is IL1B; the disease is autosomal dominant cerebellar ataxia.