Three other mouse p53 models were previously found to cause exencephaly at a higher frequency than a p53 null allele: Trp53NLS1, with three mutations at residues 316–318 affecting a nuclear localization signal and leading to a predominantly cytoplasmic localization of p53NLS1 in most cells (Regeling et al., 2011); Trp53N236S, a mouse model of TP53N239S, a recurrent but uncommon mutant in human cancers (Zhao et al., 2019); and Bim+/-Trp53-/- mice, combining p53 loss with an haploinsufficiency in the cytoplasmic proapoptotic regulator Bim/Bcl2l11 (Delbridge et al., 2019). This evidence concerns the gene BCL2L11 and cancer.