Erythroid failure caused by excess heme is independent of p53. Peripheral blood analysis of RBC, HGB, MCV, and marrow colony assays of CFU-E, BFU-E, or CFU-GM from control Trp53-null (PP ++ Mx, N = 5), Flvcr1-deleted (++ FF Mx, N = 4), or double-mutant (PP FF Mx, N = 4) mice. There was no improvement in any erythroid parameter in mice lacking both p53 and FLVCR1 compared with those only lacking FLVCR1. Analysis of 130 embryos from Flvcr1:Trp53 double-mutant breeding did not reveal any double Flvcr1-null Trp53-null embryos, whereas Trp53-null embryos were present at the expected frequency. Flvcr1-null embryos die because of failed erythropoiesis,¹⁴  and this further demonstrates that erythroid failure in mice lacking FLVCR is independent of p53. Data are presented as mean values ± SD. Differences relative to wild-type control (PP ++ Mx) mice were evaluated by 1-way ANOVA with the post hoc Tukey’s test. *P ≤ .05; **P ≤ .01; ***P ≤ .001.