Although the inhibition of PLK1 functions by small-molecule inhibitors of its catalytic activity/subcellular localization or by RNAi-mediated depletion revealed that differential levels of PLK1 are required for the viability of cancer vs. normal cells [10, 38–42], the effect of PLK1 inhibition in HGSOC cells with CCNE1-amplification remains elusive. Here, PLK1 is linked to cancer.