Administration of the porphyria-inducing chemicals allylisopropylacetamide (AIA) and 3,5-dicarbethoxy-1, 4-dihydrocollidine (DDC) to rabbits, results in the development of marked elevation of serum cholesterol, total lipids and phospholipids. The liver total lipids, cholesterol lipid phosphorus and water concentrations remain unchanged, but the organ becomes greatly enlarged, reflecting active synthesis of new protoplasm. It is suggested that these compounds affect the lipoprotein transport of serum cholesterol in a manner inducing sequestration of the synthesized cholesterol in the plasma and preventing the accumulation of cholesterol in the liver cells hence, the activation of the hepatic feed-back control for cholesterol synthesis. The possibility also exists that AIA and DDC enhances the production of one or more enzymes of cholesterol synthesis, in a way analogous to what Granick and Urata have demonstrated to occur for the enzyme δ-aminolevulinic acid synthetase of the porphyrin synthetic pathway. The chemicals, in fact, may have their primary effect on the genetic control of the rate of synthesis of different proteins by the liver. A review of the records of 51 patients with hepatic porphyria, in whom serum cholesterol determinations were recorded, reveals that hypercholesterolemia, although inconstant, is of common occurrence in the “acute intermittent” and “mixed” forms of the disease.