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The apoptosis phenomenon was identified approximately 40 years ago. In 1972, Kerr coined the term of apoptosis (programmed cellular death) to indicate that this way of cellular death was related to organic damage; but in contrast to other ways of death characterized by active cellular necrosis, in this, there is very little tissular reaction surrounding apoptotic cells. Apoptosis refers to the morphologic findings characterized by cellular shrink, nuclear condensation, fading of the membrane and fragmentation of this in apoptotic bodies with changes that possibly guide to the phagocytosis of the affected cell. Although there is great advance on phagocytosis mechanisms, signaling roads and pathology findings; a little is known about the molecular ways of apoptosis, intervening a great quantity of genes, surface receptors of T and B cells; ligand/receptor of death systems (particularly CD95), receptor of the tumoural necrosis factor (TNF-R), several interleukins with antiapoptotic activity, (specially IL-2), costimulatory receptors such as CD28 and proteins of the family Bcl-2 also with antiapoptotic activity. However, at this moment, the attention is focused in the apoptosis signaling pathways mediated by caspases, from which, 14 are known. Apoptosis has an important biological role in the development and homeostasis of cellular populations and in the pathogenesis and expression of diseases' processes. An excessive or insufficient apoptosis contributes to the pathogenesis of a wide variety of ischemic, neurodegenerative, and autoimmune diseases and viral infections, besides of participating in the growth and regression of tumoural processes. This article presents a general outline of the different apoptosis signaling pathways, the integration of multiple involved genes and receptors and the participation in several diseases of this programmed cellular death, either in excess or insufficient.