PLK4 and hepatocellular carcinoma: The incidence of spontaneous HCC in Plk4+/− mice was about 15 times higher than that of Plk4+/+ mice.32 In contrast, other studies reported that PLK4 overexpression results in centriole amplification,21, 33 while its depletion prevents centriole duplication.33 Both of the process caused loss of centrosome numeral integrity that led to aneuploidy and triggering tumorigenesis.16, 34 Thus, we speculate that PLK4 is a dose‐dependent risk factor and causes aneuploidy to promote HCC.