Noticeably, several immune checkpoints were significantly overexpressed in the S-AOIs as compared to E-AOIs, such as the T-cell-specific inhibitory receptor HAVCR2 and its corresponding tumor ligand LGALS9, or the inhibitory CD86 that interacts with CTLA4 on T-cells (Fig. 3G). The gene discussed is HAVCR2; the disease is neoplasm.