The mammalian Adenosine Deaminases Acting on RNA (ADAR) constitute a family of sequence-related proteins involved in pre-mRNA editing of nuclear transcripts through site-specific adenosine modification. ADARs are not active on adenosine-mononucleotide and are only distantly related by sequence to adenosine and AMP deaminases involved in purine metabolism. The ADARs convert certain adenosine bases in an RNA transcript into inosines by removing an amino group involved in Watson-Crick base pairing. The ADARs recognize a double stranded RNA (dsRNA) structure in the transcript that is formed between the editing site complementary sequence (ECS), usually located in the downstream 3’ intron of the transcript, and the sequence to be edited. The ADAR family of proteins consists of ADAR1 and ADAR2 which are expressed in many tissues and ADAR3 which is expressed in the brain. Regulated levels of ADAR1 expression are critical for embryonic erythropoiesis in the liver. Results show a requirement of regulated increase in the ADAR1 expression in liver at E12 and E13 stages. Failure to increase ADAR1 expression may result in underediting of the RNA of currently unknown target genes, which in turn affects proliferation and/or differentiation of erythrocytes. The absence of mature erythrocytes would lead to tissue hypoxia and the eventual death of the embryo. The best characterized target transcripts that undergo RNA editing by ADARs encode glutamate-sensitive ion channels that are expressed by neurons of the central nervous system.