Furthermore, recently developed mouse models demonstrated that induction of centrosome amplification, via transient Polo-like kinase 4 (PLK4) overexpression, not only accelerates tumorigenesis in the absence of the tumor suppressor p53 (Coelho et al., 2015, Sercin et al., 2016) but also promotes tumor formation in p53-proficient mice (Levine et al., 2017). The gene discussed is PLK4; the disease is neoplasm.