They directly affect estrogen-dependent and estrogen-independent BC cell proliferation, potentially via affecting important mechanisms, such as COX-2 inhibition or epigenetic modifications, and modulating signaling pathways, such as Hedgehog, NF-κB, Nrf2, PI3 kinase, Plk1, poly-ADP-ribosylation, STAT3, Wnt, and others [49]. This evidence concerns the gene PLK1 and breast cancer.