Other NSAIDs, such as sulindac, can also mediate the antiproliferative degradation of β-catenin in cancer cells partly by proteasomal degradation and partly by caspase-mediated cleavage [150], whilst others such as diclofenac have been shown to suppress Wnt/β-catenin/TCF signalling via the activation of NF-κB [127]. Here, NFKB1 is linked to cancer.