Other notable processes that were revealed through GO analysis included widespread enrichment of protein folding and prion disease terms, as well as signaling cascades implicated in FMR1 pathophysiology [including Wnt signaling, phosphoinositide 3 kinase (PI3K) signaling, and MAPK signaling (33, 51, 52)] in both neurons and glia in both premutation and FXS comparisons in multiple populations (SI Appendix, Supplemental Information Files 1 and 2). The gene discussed is FMR1; the disease is fragile X syndrome.