SREBPs serve to regulate all 12 enzymes in the cholesterol biosynthetic pathway including the rate limiting enzyme HMGCoA reductase (HMGR). High dietary sterol levels acting on SCAP ultimately stop the maturation of SREBPs, resulting in the down regulation of key enzymes such as HMGR, thus, reducing the amount of cholesterol produced by the liver. Limiting cholesterol synthesis leads to a homeostatic response in which cells increase the density of LDL receptors on their surfaces. This increases the clearance rate of LDL particles from the plasma and reduces plasma LDL cholesterol and its related health risks. The decrease in cholesterol synthesis also promotes an increase of HDL, thus, clearing even more cholesterol from the plasma.