At least in the United States, this XL-SCID ("X-SCID") is the most frequent SCID; it is an exclusively immunological form except that also cutaneous keratinocytes express γc-dependent cytokine receptors and the associated JAK3 (see later), and these is necessary for the local innate immunity of keratinocytes against human papilloma virus (HPV); therefore, severe cutaneous HPV disease, including epidermodysplasia verruciformis, is a frequent late complications in common γc (and JAK3) SCID patients many years after successful HSCT or gene therapy [48]. The gene discussed is JAK3; the disease is epidermodysplasia verruciformis.