In addition to the LDLR gene augmentation approach, the successful use of the VLDLR as an effective surrogate lipoprotein receptor gene [139-141,153,216,217] for the complementation of mutated LDLR function in homozygote FH patients would also open an alternative therapeutic avenue, since it would avoid the immune problem in patients with no natural LDLR. The gene discussed is LDLR; the disease is familial hyperaldosteronism.