“…Genes that were strongly upregulated in syndromes with both cutaneous and mucosal involvement were those involved in inflammation, now termed alarmins or endogenous damage-associated molecular patterns. 9 In a study by Tohyama et al, immunostaining of cryosections from SJS and TEN lesions revealed CD141 monocytes in the dermoepidermal junction, and CD141 CD161 cells present early in the disease process, before epidermal damage occurred, suggesting that the monocyte ''infiltration is a cause, rather than a result, of epidermal damage.'' 10 Merk discusses the role of xenobiotica-metabolizing enzymes and transport proteins as a biochemical barrier that serves, in addition to the epidermal stratum corneum, as a protection from toxic chemical compounds.…”