Background: Acne vulgaris is a disease of the pilosebaceousunit. Increased sebum lipogenesis by sebaceous gland is themajor factor in the pathophysiology of acne. LXRα have beenrecognized in the regulation of genes involved in lipidbiosynthesis. Activation of LXRα inhibits proliferation, increaselipogenesis and improve differentiation of sebocytes.Aim: To investigate the level of tissue expression of LXRα ininflammatory and non inflammatory acne lesions and incomparison with normal skin.Patients and methods: Seventeen patients with inflammatoryand non inflammatory acne lesions and sixteen age and sexcomparable healthy volunteers as control were included in thestudy. Punch skin biopsies were taken from the acne lesions andnormal skin of the volunteers for detection of gene expression ofLXRα by RT- PCR.Results: the level of LXRα was significantly higher in thelesional skin either inflammatory (with a mean of 1188.52 ±129.5) or comedonal acne (with a mean of 892.52 ± 66.08) in astatistically significant manner than the controls (with a mean of600.50 ± 95.30) where the P value was <0.001. In addition, the level of LXRα was significantly higher in inflammatory acne(with a mean of 1188.52 ± 129.5) in a statistically significantmanner) than comedonal acne (with a mean of 892.52 ± 66.08)where the P value was <0.001.Conclusion: the significant increase in the level of LXRα in acnelesions compared to controls suggesting that LXRα may have arole in the pathogenesis of acne vulgaris itself and is not aconsequence of inflammation. In addition, it may play a role inthe progression of the disease from comedonal to inflammatory.Further studies are recommended to evaluate the therapeuticbenefits of the use of LXRα antagonists as a new therapeuticmodality for acne vulgaris.