TP53 and Treacher-Collins syndrome: In TCS, apoptotic elimination of neuroepithelial cells and neural crest cells upon p53 activation mediated by the nucleolar stress response has been considered to be the primary cause of craniofacial anomalies in TCS.177 Genetical or pharmacological inactivation of p53 can rescue disease-associated phenotypes, strongly supporting that p53 is a key molecular mediator of the hypo-proliferative clinical symptoms of ribosomopathies.18,19,126,127