The expression levels of IFN-γ, IL-3, IL-13, IL-5, IL-21, granulysin and granzyme B, all of which have been associated with pathogenesis of SJS and DDS-DIHS [48–52], were elevated in the DDS-expanded T cells expressing the aforementioned TCR clonotypes (Fig. 4G), further suggesting that these TCR clonotypes are involved in the pathogenesis of DDS-DIHS. Here, IL3 is linked to Denys-Drash syndrome.