Indeed, PLK1 haplo-insufficient mice displayed widespread aneuploidy accompanied by a higher incidence of tumor formation [39], and inhibition of PLK1 in an adenomatous polyposis coli protein (APC)-truncated context impaired SAC function and led to increased CIN and tumor formation [214], reminiscent of a tumor suppressor-like function in tumorigenesis. Here, APC is linked to neoplasm.