Given the critical role of CCND2 and IRF5 in cell cycle regulation as growth-inhibitors [18,20], our data here account for the functional significance of FBXL8 as a tumor-promoter, whose knockdown spared the tumor suppressors, CCND2 and IRF5 from degradation, thus allowing them to accumulate and suppress BRCA progression. The gene discussed is IRF5; the disease is neoplasm.