Currently, gene therapy approaches have mainly focused on two of the most common types of SCID: the autosomal recessive inherited enzymatic defect of the ubiquitously expressed adenosine deaminase (ADA-SCID) that plays role in the purine salvage pathway, and the dysfunction in interleukin-2 (IL-2) signalling due to mutations in the X-chromosomal encoded common gamma chain of the IL-2 receptor (SCID-X1; Aiuti et al, 2009; Candotti et al, 2012; Cavazzana-Calvo et al, 2012; Fischer et al, 2013; Gaspar, 2012; Hacein-Bey-Abina et al, 2002). This evidence concerns the gene ADA and severe combined immunodeficiency.