ALS-Glia upregulation of CHI3L2, CX3CR1, FOLH1, HLA-DRA, ALOX5AP, CCR5, CR1, FPR3, NCF2, TLR8, and TNFRSF25 generally indicates a pro-neuroinflammatory and pro-apoptotic disease phenotype30,31,38–46 (Fig. 6 and Fig. S9). Here, CX3CR1 is linked to amyotrophic lateral sclerosis.