Earlier study has proved that overexpressed β-catenin can actually interact with NF-κB indirectly and hamper its activity, signifying a narrative mechanism for β-catenin-mediated oncogenesis; namely, β-catenin hampers NF-κB activity, which may permit cancer cells to flee immune scrutiny and also the study stalwartly proposed that β-catenin is a chief mediator for the cross regulation of NF-κB by the GSK-3β pathway [61]. Here, GSK3B is linked to cancer.