In our prior studies, we have shown that hypercholesterolemia observed in experimental CRF is partially caused by the enhanced cholesterol biosynthesis associated with the up-regulation of Srebf-2 and Hmg-CoA reductase genes expression as well as by a decrease in LDL-receptor (LDL-R) mRNA level [3–5]. This evidence concerns the gene LDLR and familial hypercholesterolemia.