One explanation for this paradoxical behavior, CIN itself can impede tumor growth due to the increased defect burden, and so reducing this CIN burden contributes to increased cell growth, This could explain inconsistent results regarding the effect of PLK1 on tumor initiation versus tumor inhibition, with some studies showing PLK1 driving oncogenic transformation and increased growth advantage but others showing PLK1 overexpression decreasing tumor initiation rates [107,213,214,215]. Here, PLK1 is linked to neoplasm.