Drug-induced TEN implicates multiple distinct pathways, most notably Fas-Fas ligand interactions on keratinocytes, high levels of circulating soluble Fas-Fas ligand, reactive oxygen species-mediated direct keratinocyte toxicity, and, to a lesser extent, direct cell-mediated killing by cytotoxic T cells and natural killer cells. The gene discussed is FAS; the disease is toxic epidermal necrolysis.