In our analysis, we observed similar results, where upregulated DEGs in tumor regions of both Glio-IDH-wt and Glio-IDH-mut exhibited enrichment in pathways such as PI3K/Akt, human papillomavirus infection, cytokine-cytokine receptor interaction, human T-cell leukemia virus 1 infection, cytoskeleton in muscle cells, focal adhesion, human cytomegalovirus infection, regulation of actin cytoskeleton, and human T-cell leukemia virus 1 infection. The gene discussed is AKT1; the disease is neoplasm.