To assess the impact of centrosome amplification on CIN, senescence, lifespan and tumor formation in vivo with an orthologous approach without interfering with PLK4, we generated transgenic mouse models overexpressing the structural centrosome protein STIL, a 1,288 amino acid protein that is recruited to the proximal end of the mother centriole after phosphorylation by PLK4 to mark the procentriole emergence site [1]. The gene discussed is PLK4; the disease is neoplasm.