Firstly, transduction of IPEX patient conventional T cells with a lentiviral vector (expressing FOXP3 under a constitutive EF1a promoter) converted them to potent Treg like suppressor cells but this approach does not address the defect in other cell types such as T effector cells themselves which contribute to the pathophysiology of IPEX syndrome (Goodwin et al., 2020). The gene discussed is FOXP3; the disease is immune dysregulation-polyendocrinopathy-enteropathy-X-linked syndrome.