RAG1 and Omenn syndrome: On the other hand, a frameshift indel would introduce premature early stop codons interrupting the expression of the full-length RAG1 protein, modeling the genetic defects that fully abolish the function of RAG1 (a RAG1-null or KO genotype) as observed in more extreme forms of SCID; it is also possible that a frameshift indel in the non-core domain may still allow the alternative usage of other Mets (ATG) downstream of the indels as translation start codons to produce N-terminal truncated RAG1 with partial VDJ recombination activities, as observed in some Omenn syndrome patients [16].