The fact that in the latter case no apoptosis was detected26 is consistent with reports showing that UPR and ER stress, which characterizes Elp3 microcephaly,26 may activate mechanisms capable of preventing P53-dependent death.58, 59 Nevertheless, P53 activation and transcriptional induction of some P53 targets can still be sufficient to induce the growth arrest detected in Elp3-deficient neural progenitors.26 Here, TP53 is linked to microcephaly.