AbstractElevated levels of cholesterol are known to be a risk factor for cardiovascular diseases. As a result, several treatment strategies and drugs have been developed to control these elevated cholesterol levels, but they are not always successful. A dynamic mathematical model of the cholesterol biosynthesis network was developed with aim to understand the key mechanisms of cholesterol biosynthesis. Cholesterol biosynthesis is a complex system of metabolic pathways and control mechanisms that interact on many levels. The basis represents a metabolic pathway that starts at the Krebs cycle (cell breathing) and forms cholesterol in several steps. Some intermediates lead to other important substances, such as co-enzyme Q, vitamin D, corticosteroids, setc. To maintain the levels of many metabolites that are produced by the same metabolic pathway, a sort of cascade control with hierarchical arrangement must be used. The level of the most important metabolite has the higest priority in control action. The control mechanism for cholesterol biosynthesis operates mainly on two levels. One is the transcription level, where the rate of DNA transcription to mRNA is controlled. The other is degradation of enyzmes involved in cholesterol biosynthesis. In case of elevated cholesterol levels cholesterol can mediate degradation of practically all cholesterogenic enzymes. In this paper we focused on transcriptional regulation of cholesterol biosynthesis. The control mechanism for the cholesterol levels through the SREBF-2 transcription factor was identified as the PI control algorithm. There are many consequences that can be drawn from the shown analysis. As it seems, all the proposed strategies that were focused on liver metabolism of cholesterol or cholesterol uptake from the intestine were only trying to remove the consequences but not the origin of the cholesterol levels imbalance.