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Abstract Acne vulgaris is a chronic inflammatory skin disease of pilosebaceous units affecting skin areas with dense population of sebaceous follicles such as the face, upper chest and back. Acne is characterized by non-inflammatory (open or closed comedones) and inflammatory lesions (papules, pustules, or nodules). Mammalian target of rapamycin is a nutrient‐sensitive regulator of cellular growth and proliferation, lipid synthesis and protein translation, exerting its effects through two distinct signaling complexes: mTORC1 and mTORC2. In particular, rapamycin‐sensitive mTORC1 promotes cell growth and proliferation, which may translate into proliferation of acroinfundibular keratinocytes and increased lipid biosynthesis in sebaceous glands, which are responsible for seborrhea. Conversely, mTORC2, which is non-sensitive to rapamycin, is involved in the regulation of cell polarity and in the functional phosphorylation of cytoskeleton actin fibers. Multiple diseases, either neoplastic, dysmetabolic or inflammatory, show dysregulation of mTOR pathway, which might be also involved in inflammatory skin diseases such as psoriasis, atopic dermatitis and allergic contact dermatitis. Acne appears to develop in metabolic environments with increased mTORC1 signaling, and has been proposed to represent a visible mTOR‐driven disease of civilization.The aim of this study was to use mTOR gene expression as a prognosticmolecular marker to detect severity of acne, minimize complication and improvequality of life. - |