The results revealed that 35 pathways including Systemic Lupus Erythematosus, Autoimmune Thyroid Disease, Allograft Rejection, Antigen Processing and Presentation, P53 Signaling Pathway, and Glycosaminoglycan Degradation were significantly activated (p < 0.05) in highly RAB42 expressed GBM patients, compared with low RAB42 expression samples (detailed results were listed in Table S2). The gene discussed is TP53; the disease is autoimmune thyroid disease.