Enhancer elements of the long terminal repeats (LTRs) retained in these vectors used as a possible treatment for severe combined immunodeficiency (SCID)-X1, and Wiskott-Aldrich Syndrome (WAS), led to insertional mutagenesis of host genes, particularly LMO2, causing increased levels of transcription and protein [4–7]. The gene discussed is LMO2; the disease is Wiskott-Aldrich syndrome.