As errors in ribosome biosynthesis activate the RPL5/RPL11/5S rRNA/HDM2/p53 signaling pathway, it has been suggested that the selection of cells that loose expression of wild-type p53 or acquire mutations in p53 or other signaling components of the RPL5/RPL11/5S rRNA/HDM2 complex may allow escape from the ribosome biogenesis stress-imposed checkpoint, thereby facilitating tumor progression. This evidence concerns the gene TP53 and neoplasm.