Since PLK1 possesses a key role for centriole duplication and G2/M transition in cell cycle [58, 59], identification of this kinase in the same signaling cascade together with CEP135, pathway that was shown by us to be activated in subgroup of sarcoma with high CEP135 expression, supports PLK1 as a plausible target candidate. The gene discussed is CEP135; the disease is sarcoma.