GFAP and cerebellar ataxia: GFAP was enriched with the JAK/STAT signaling pathway (Supplementary Figure S6), C4A was enriched with the pathways such as JAK/STAT signaling, cytokine-cytokine receptor interaction, B cell/T cell receptor signaling (Supplementary Figure S7), VDAC1 was enriched with neurodegeneration pathways of multiple diseases such as Alzheimer’s, Parkinson’s, Amyotrophic lateral sclerosis, Huntington’s, Spinocerebellar ataxia, and Prion’s (Supplementary Figure S8), and the ADCYAP1R1 gene was enriched with neuroactive ligand–receptor interaction pathway (Supplementary Figure S9).