Considering the almost identical degree of severity of anemia in Agt(-/-), Ren(-/-) (in this study) and ACE knockout mice (previously reported in [40]), we speculate that the anemic phenotype observed in these animals is attributable to complete loss of Ang II production, rather than the accumulation of substrates of or the loss of products (other than Ang II) of ACE or renin enzymes, because Ang II and its fragments, such as Ang (1–7) or Ang III, are the only common peptides produced from angiotensinogen, renin, and ACE. The gene discussed is AGT; the disease is anemia (phenotype).