We further investigated the function of AKR1B1 in glioma tissues using GSEA and found that interferon gamma signaling, signaling by interleukins, cell cycle checkpoints, cytokine receptor interaction, cell adhesion molecules (CAMs), and cell surface interactions at the vascular wall all showed significantly differential enrichment in high AKR1B1 expression phenotype. The gene discussed is IFNG; the disease is glioma.