with development of the DRESS syndrome in response to certain drugs, have developed tests to identify individuals who express some of these serotypes, and thereby have identified individuals who should avoid certain DRESS syndrome-inducing drugs. T-cell receptors A drug or its metabolite may also stimulate CD8+ T or CD4+ T cells to initiate autoimmune responses by directly binding to the T-cell receptors on these T cells. Again, this binding appears to develop only on certain T-cell receptors. Since the genes for these receptors are highly edited, i.e. altered to encode proteins with different amino acid sequences, and since the human population may express more than 100 trillion different (i.e. different amino acid sequences) T-cell receptors while an individual express only a fraction of these, a drug's or its metabolite's ability to induce the DRESS syndrome by interacting with a T-cell receptor is limited to those individuals whose T cells express a T-cell receptor(s) that can interact with drug or its metabolite. Thus, only rare individuals are predisposed to develop a SCARs disorder in response to a particular drug on the basis of their expression of specific cell receptor types. While the evidence supporting these ideas is limited, one study identified the preferential presence of the TCR-V-b and complementarity-determining region 3 in T-cell receptors found on the T cells in the blisters of patients with allopurinol-induced DRESS syndrome. This finding is compatible with the notion that specific types of T-cell receptors are involved in the development of specific drug-induced SCARs. ADME Variations in ADME, i.e. an individual's efficiency in absorpting, distributing, metabolizing, and excreting a drug has been found to occur in cases of the DRESS syndrome. These variations influence the levels and duration of a drug or drug metabolite in tissues and thereby impact the drug's or drug metabolite's ability to evoke the DRESS syndrome. For example, the CYP2C9 gene codes for CYP2C9, a cytochrome P450 enzyme which metabolizes various substances including phenytoin. The CYP2CP*3 variant of CYP29C has reduced catalytic activity; individuals expressing this variant show an increased incidence of developing the DRESS syndrome when taking phenytoin apparently due to increases in the drug's blood and tissue levels. In a second example of a genetically based ADME defect causing SCARs, Japanese individuals bearing slow acetylating variants of the N-acetyltransferase 2 gene, (NAT2), viz., NAT2*6A and NAT2*7B, acetylate sulfasalazine more slowly than individuals homozygous for the wild type gene. Individuals