**5. Conclusions**

Over 40 years have passed since the first publication devoted to apoptosis. Since then, the problem of apoptosis regulation mechanisms has become central to pharmacology, genetics, virology, cytology, immunology, biochemistry, embryology, and other areas of modern science at the cellular and molecular levels. It is obvious that the problem addressed in this chapter is of high applied value, for the key aim of the effort is to enhance the effectiveness of anticancer therapy. The industry of rational drug design is becoming more and more widespread in practical medicine. The principal concepts in drug design are the target and the drug. The target is a low-molecular biological structure presumably linked to a certain function which disruption would lead to disease, and to which a certain impact should be applied. The most common targets are receptors, enzymes, hormones. The drug is most often a chemical compound (usually a low-molecular one) that specifically interacts with the target, modifying the cell response in one way or another. One of the earliest and most seminal stages of drug design is accurate identification of the target by influencing which one can specifically regulate certain biochemical processes, leaving others unaffected as much as possible. This is not however always feasible: by no means are all diseases caused by dysfunction of just one protein or gene. Preference should therefore be given to the processes' principal biomolecules. In terms of apoptosis, caspases clearly are such biomolecules. Hence, the choice of methods for experimental validation of caspases as potential specific targets for drugs is a topical challenge for the nearest future.
