A previous in vitro study showed that inhibition or knock down of PLK1 in six cancer cell lines led to increased histone H3 phosphorylation (pHisH3) at 6 h followed by increased γ-H2AX expression at 24 h and increased PARP cleavage at 24–48 h, with senescence occurring in some of these cell lines after 2 weeks [29]. The gene discussed is H2AX; the disease is cancer.