According to this theory, the culprit drug sets in motion an immune response mediated by MHC, with the clonal expansion of CD8+ T cells and interleukin-2 (IL-2) secretion, followed by keratinocyte apoptosis that can occur in two phases: one guided by T cells, as it happens in other dermatological adverse drug reactions, and that is highly dependent on granulysin and cellular death pathways; and another with response amplification that is specific to TEN [2]. This evidence concerns the gene HLA-C and toxic epidermal necrolysis.