Here, through re-introduction of FBXW7 in FAM83D overexpressed MCF7 cells or knockdown of FBXW7 in FAM83D silenced BT549 cells, we found that augmented FBXW7 ameliorated the stimulative effects of FAM83D on cell proliferation, migration and invasion whereas FBXW7 ablation nearly reversed the anti-tumor phenotype induced by FAM83D deficiency, indicating that FBXW7 mediates the function of FAM83D on cell growth and mobility in BC. Here, SACK1D is linked to breast cancer.