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Abstract Alopecia areata is a disfiguring disease characterized by nonscarring hair loss on the scalp or other parts of the body. It is characterized by sudden loss of hair in rounded or oval shaped single or multiple patches with spontaneous remission, relapse, and exacerbation. AA can develop into more severe forms; AT which involves loss of all scalp hair and AU which means complete loss of all body hair. Most evidence suppports the hypothesis that AA is a Tcell mediated autoimmune disease of the hair follicles. Alopecia areata has a multifactorial etiology so that several genes and environmental factors come together with a different weight in triggering the pathology. Moreover, AA clusters in families; 10 25 % of all patients have affected relatives. Apoptosis is an essential process in immune homeostasis and regulation, and it is particularly important in the termination of immune responses. Defects in the elimination of cells or in the processes can contribute to the breakdown of tolerance and development of autoimmunity. FAS and FASL are important proapoptotic proteins, which belong to the tumor necrosis factor superfamily and play essential roles in many human autoimmune diseases. The human FAS gene is located on chromosome 10q24.1 while the human FASL gene is located on chromosome 1q23. A to G substitution at position 670 in the promoter region of FAS may destroy the binding elements for stimulatory protein 1(Sp1) and signal transducer and activator of transcription protein 1 (STAT1), thus leading to decreased promoter activity and FAS expression. |