Since FBXL8-knockdown raised the levels of CCND2 and IRF5, which resulted in cancer suppression, it is conceivable that as a tumor-promoter, FBXL8 acts as a dominant member of a tripartite liaison, in which FBXL8 controls the protein level and functionality of the two tumor suppressors, CCND2 and IRF5 (Figure 6). The gene discussed is IRF5; the disease is neoplasm.