In support of this, the list of 210 genes by Fischer et al. (2016a) included only one gene mutated in Fanconi anemia (Fancb) and no genes mutated in dyskeratosis congenita, whereas in a previous study with mouse fibroblasts focusing on these bone marrow failure syndromes (Jaber et al., 2016), we found evidence for the p53-mediated repression of eight clinically relevant genes that belong to our current list of 151 targets (Fanca, Fancb, Fancd2, Fanci, Palb2, Rad51, Rtel1 and Ube2t). Here, RAD51 is linked to dyskeratosis congenita.