TBXT and toxic epidermal necrolysis: Ample evidence suggests that HLA is directly involved in drug hypersensitivity.19 HLA molecules present antigenic drugs to the T-cell receptor, causing clonal expansion and activation of CD8+ cytotoxic T cells.20 A pharmacogenomics study found an unusual form of granulysin to be secreted by these cytotoxic T lymphocytes and found natural killer cells to be responsible for the rapid and disseminated keratinocyte death observed in diseases such as Stevens–Johnson syndrome and toxic epidermal necrolysis.16