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 Here, CD8A is linked to toxic epidermal necrolysis.