WAS and juvenile Huntington disease: As for KEGG pathways, ACTN1, TLN1, F5 and WAS were mainly enriched in immune-related pathways, such as chemokine signaling pathway, B cell receptor signaling pathway, Fc gamma R-mediated phagocytosis, antigen processing and presentation (Figure 10A–10D), while JMJD1C was more likely participated in pathways related to neuroinflammation, such as Alzheimer’s disease, Huntington’s disease and oxidative phosphorylation (Figure 10E).