Inhibition of HMG CoA reductase reduces intracellular cholesterol levels; this activates a protease, which in turn cleaves SREBPs from the endoplasmic reticulum. The SREBPs translocate to the nucleus where they upregulate expression of the LDL receptor gene. Enhanced LDL receptor expression increases receptor-mediated endocytosis of LDL and thus lowers serum LDL. Inhibition of HMG CoA reductase also reduces intracellular levels of isoprenoids, which are intermediates in cholesterol biosynthesis.