THE results of studies in which L-gulonolactone-1-14C, the precursor of L-ascorbic acid in the rat, was administered to guinea-pigs showed that the guinea-pig is apparently unable to synthesize vitamin C1-3. This has been attributed to the absence of gulonolactone oxidase from the liver microsomes of the guinea-pig; because this enzyme is the last one in the series for converting glucose to ascorbic acid it completely blocks endogenous synthesis. Synthesis of ascorbic acid has been demonstrated in rats: gulonolactone oxidase is present in their livers4-6. A defect, probably a conditional lethal mutation7, in the gene controlling the synthesis of this enzyme in guinea-pigs produces an inactive enzyme or its complete absence. They are therefore dependent on exogenous vitamin C. This genetic disease has been named hypoascorbemia because of the low levels of ascorbic acid in the blood which are pathognomonic of the condition8. Neither the sex nor the age of the animals in these experiments was stated, and there was no indication of the state of ascorbic acid tissue saturation or of the scorbutic condition of the guinea-pigs.