At therapeutic concentrations (100–200 μM, achievable via intratumoral delivery), I3A activates the AhR/cAMP response element-binding protein (CREB) axis in CD8+ T cells: specifically, AhR recruits CREB to the IFN-γ promoter, inducing CREB phosphorylation at Ser133 to amplify type 1 cytotoxic T cell (Tc1) differentiation and tumor cytotoxicity (113, 171). The gene discussed is CREB1; the disease is neoplasm.