The current paradigm for TEN onset states is that, once they have been primed in lymphoid organs, drug-specific cytotoxic CD8+ T cells (CTLs) are recruited at the dermo-epidermal junction where they kill keratinocytes presenting drug epitopes at their surface, through mechanisms involving perforin/granzyme B and MHC class I–restricted pathways (6, 10). This evidence concerns the gene CD8A and toxic epidermal necrolysis.