Simultaneously, IRF2 and POU2F1 re-engagement in the tumoral compartment, when β-catenin is suppressed, acts as a mediator of enhanced interferon network signaling and primes lymphocyte recruitment and infiltration, with all these tumor-intrinsic and TIME remodeling mechanisms ultimately driving synergy with β-PD1 in the advanced-stage disease setting. This evidence concerns the gene IRF2 and neoplasm.