Apoptosis or programmed cell death is genetically determined process to destroy cells for the maintaining of cellular homeostasis in the tissue. This paper reviews the current knowledge on the molecular mechanisms of apoptosis. Activation of cysteine proteases called caspases plays a major role in the execution of apoptosis. These activated caspases selectively cleave cellular proteins, which result in apoptotic morphology (internucleosomal fragmentation of DNA into 180-200 base pair pieces, shrinkage of the cell and the nucleus as well and fragmentation of the cell into apoptotic bodies) and death of the cell. Now two pathways of caspase activation are reported. The first through triggering of cellular death-receptor superfamily. The second is mitochondrial pathway induced by the changes of the expression of pro- and anti-apoptotic genes in the cell. It leads to release of cytochrome c and apoptosis inducing factor from mitochondria. The paper reviews also currently used methods of detection of apoptotic cells in tissue samples, causes of false-positive or false-negative results of ISEL and TUNEL in situ reactions.