IN THIS age of genetic engineering and transgenic and knockout mice, it is sobering to realize that the immunopathogenesis of psoriasis was discovered largely through clinical research in patients with psoriasis. Before the mid-1980s, the keratinocyte was the focus of scientific research in psoriasis because both the clinical and histologic phenotypes of this disease are dominated by the results of abnormal keratinocyte proliferation and differentiation.1-6 However, the results of research since then have demonstrated that if one eliminates the activated T lymphocyte in psoriatic plaques, keratinocyte proliferation and differentiation return to normal both clinically and histologically.7-10 Thus, the abnormalities in the keratinocytes are reversible. Clinically, psoriatic plaques are described as red, elevated, and scaly. Both the elevation and scale are direct results of the same altered keratinocyte proliferation and differentiation that have been observed in acute and chronic cutaneous wounds. This alternate pathway of keratinocyte differentiation has been