Genetic aberrations in several NHEJ pathway constituents, such as prkdc, dclre1c, rag1/rag2, Ku70/80, XRCC4 and Ligase IV, have been associated with the manifestation of SCID, typified by the concurrent deficiency of T and B cells [31,32,33]. This evidence concerns the gene RAG2 and severe combined immunodeficiency.