CDKN2A and cancer: Although further studies are warranted to explore precisely the molecular pathways through which disruption of the pRB/p16INK4a axis leads to centriole amplification in the presence of telomere-dependent genotoxic stress, our work has uncovered a mechanistic link for the coincident detection of telomere erosion and centrosome aberrations early in cancer development, before TP53 mutations are gained.