Pimecrolimus is an ascomycin and macrolactam derivative, acting as a calcineurin inhibitor which binds calcineurin (Dissemond et al, 2002). The consequence of calcineurin binding is a lack of activation of both T helper cell types 1 and 2. Further effects of these compounds have been suggested on other inflammatory cells, such as Langerhans cells and mast cells/basophils. Both entities, dLE and scLE are characterized by B-cell activation due to affected T-cell activation and the formation of multiple autoantibodies. This results, among other symptoms, in inflammatory infiltrates, especially on the face. Pimecrolimus cream is already approved for the treatment of atopic dermatitis. Furthermore, there have been studies in other indications like psoriasis, allergic and irritant dermatitis. Pimecrolimus has been developed for the potential treatment of psoriasis, allergic, irritant and atopic dermatitis. Animal studies with tacrolimus ointment cream used for lupus dermatoses have shown to be promising (Neckermann et al., 2000; Meingassner et al. 1997; Bochelen et al. 1999). Topical tacrolimus therapy was applied to facial skin lesions in 7 cases of cutaneous lupus erythematosus (cLE). Three systemic LE and one discoid showed a marked regression of their skin lesions after tacrolimus therapy, but three patients with discoid LE were resistant to the therapy. A good response was observed for facial erythematosus lesions with edematous or telangiectatic changes in systemic LE (Yoshimasu et al, 2002, Furukawa et al., 2002). In discoid LE with typical discoid lesions, tacrolimus brought no improvement. Pimecrolimus seems to be more promising than tacrolimus due to the altered skin penetration profile. Topical pimecrolimus cream, in contrast to corticosteroids, does not provoke any skin atrophy (Dissemond et al., 2002; Queille-Roussel et al.; 2001) and might be a good alternative to the standard treatment of potent corticosteroids, even if only a part of the patient population will respond to Elidel® treatment.