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Previous Volume 334:802-803 March 21, 1996 Number 12 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: In the study by Bosma et al. (Nov. 2 issue)¹ of the genetic basis of Gilbert's syndrome, the relevance of the variant TATAA element is far from certain. The authors do not provide data or cite references that demonstrate that a quantitative reduction in bilirubin UDP-glucuronosyltransferase 1 (bilirubin/uridine diphosphoglucuronate-glucuronosyltransferase 1) in patients with Gilbert's syndrome is related to transcriptional rather than translational or post-translational mechanisms. Furthermore, the normal functional characteristics of the native promoter are not made clear. Is transcription regulated by constitutive or inducible mechanisms? this point is relevant because the experiments were restricted to four . . . [Full Text of this Article]

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