The risk of insertional mutagenesis and oncogene transactivation associated with this generation of GT vectors prompted the development of safer, self-inactivating lentiviral vectors (SIN-LV), hence subsequent clinical trials for the treatment of WAS transitioned to the use of SIN-LV expressing WAS under the control of its endogenous promoter, offering a potentially safer and more physiological expression of WASp. This evidence concerns the gene WAS and Wiskott-Aldrich syndrome.