Kim et al. [21] found that FSTL1, downregulated in the MSC secretome from patients with cerebellar ataxia, could serve as an anti-inflammatory cytokine with suppressive effects on proinflammatory microglial activation. Paradoxically, it is worth noting that FSTL1 has been identified as a novel inflammatory protein that enhances the ability of monocytes/macrophages to respond to inflammatory signals [16, 17, 22]. This evidence concerns the gene FSTL1 and cerebellar ataxia.