GPR109A and GPR43 are involved in the binding of β-arrestin, some of which are related to the inhibition of nuclear factor-kappa-gene binding (NF-κB), β-arrestin-2 directly interacts with NF-κB inhibitor (IκBα), preventing the phosphorylation and degradation of IκBα.134 However, this pathway is mainly related to anti-inflammatory and desensitizing effects,118,120 and its role in cancers is still unclear. This evidence concerns the gene NFKB1 and cancer.