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In multicellular organisms, homeostasis is maintained by a balance between cell proliferation and cell death. Two common forms of cell death, called apoptosis and necrosis, have been described. Apoptosis, which is often equated with programmed cell death, is a physiological form of cell death that is responsible for the deletion of cells. Apoptosis is morphologically and biochemically characterized by cell shrinkage, dense chromatin condensation, cellular budding, fragmentation, rapid phagocytosis by nearby cells, and DNA fragmentation into units of approximately 200 base pairs. Apoptosis can be triggered by a wide variety of stimuli such as cytokines, hormones, drugs, and viruses, and their signal transduction tightly regulated by genes such as Bcl-2. Effector caspases are finally activated, resulting in apoptotic cell death. In the skin, there is considerable evidence that apoptosis plays an important role in the pathogenesis of a wide variety of skin diseases. In lichenoid tissue reactions, the Civatte body or colloid body is a form of apoptotic keratinocytes which is mediated by T lymphocytes via Fas-FasL interaction or through the perforin-granzyme B pathway. In several skin tumors, Bcl-2 or FasL expression is involved in the proliferation or regression of the tumors, or in the escape from immune attack by T cells. Moreover, apoptosis is also responsible for the homeostasis of skin, such as the keratinocyte differentiation and hair cycle. In this review, we describe the basic concept of apoptosis and its relevance to skin diseases.