Three classes of hypolipidaemic drugs are used currently for the prevention of cardiovascular diseases. Resins, by binding bile acids, prevent the intestinal reabsorption of these acids. Subsequently, an increase in their synthesis appears to arise from intracellular cholesterol. The intracellular cholesterol concentration decreases and leads to an increase in the number of LDL receptors. The consequence is a decrease in plasma LDL-cholesterol level. Statins act by inhibiting HMGCoA reductase, a key enzyme which regulates intracellular cholesterol synthesis. Thus, the intracellular cholesterol level decreases and leads to an activation of SREBP2 (Sterol regulatory element-binding protein), a transcription factor which, by binding to the promoter of the LDL-receptor gene, activates its transcription and thus the numbers of LDL receptors. The final effect is a decrease in plasma LDL-cholesterol. Fibrates activate a transcription factor named PPAR alpha. This activation results in binding with RXR, another transcription factor. The PPAR alpha/RXR heterodimer binds to the promoter of specific genes increasing their transcription and thus the proteins coded by these genes. This mechanism accounts for the increase in lipolysis (modulation of apoCIII and lipoprotein lipase) and in HDL-cholesterol (modulation of apoAI and apoAII genes).