Despite this versatility, ICA’s pan-cancer potential is limited by AhR activation thresholds: in tumors with AhR overexpression (e.g., glioblastoma, pancreatic cancer), its weak agonistic activity may paradoxically sustain immunosuppression by reinforcing AhR-mediated pro-tumor signaling, rather than exerting antagonistic effects. The gene discussed is AHR; the disease is familial pancreatic carcinoma.