To summarize, GSEA indicates that, in CRC, TIGIT primarily marks an immune-inflamed program, with the highest enrichment clustered around interferon signaling (IFN-g/IFN-a) and broader inflammatory cytokine axes (TNFa/NF-kB, IL6-JAK-STAT3), while the most depleted signatures group into tumor-intrinsic growth/metabolic programs (notably MYC targets and oxidative phosphorylation). The gene discussed is STAT3; the disease is colorectal carcinoma.