Patients with several clinically distinctive types of cutaneous LE (e.g., SCLE, neonatal LE) frequently are found to have autoantibodies to the Ro RNP particle present in their circulation. Some studies suggest that these antibodies might be capable of directly triggering the type of histopathologic changes seen in SCLE and neonatal LE through immunologic effector mechanisms such as ADCC. Other investigative results, however, are not compatible with this hypothesis. A better understanding of the molecular configuration of the Ro small cellular RNP particle, the factors that regulate the expression of this complex autoantigen system in epidermal keratinocytes, and the overall pathogenetic potential of the Ro autoimmune response should provide some insight into this seeming paradox.