In conclusion, our results demonstrated that in SCA pathophysiology at steady state, there is a broad immunological biomarker crosstalk highlighted by TCD4+ lymphocytes; TLR2 in monocytes; VLA-4 in TCD8+ lymphocytes; Th1, Th17 inflammatory, and IL-10 regulatory cytokines; MIP-1α, MIP-1β, and IP-10 chemokines; and growth factor VEGF. This evidence concerns the gene CCL3 and autosomal dominant cerebellar ataxia.