"The rapidity and simplicity of this test suggests that it would be useful as a clinical laboratory procedure for diagnosing sickle cell anemia and sickle cell trait."

Linus Pauling. "A Rapid Diagnostic Test for Sickle Cell Anemia," Blood, 4(1): 66-68, 67. January 1949.

"It appears, therefore, that while some of the details of this picture of the sickling process are as yet conjectural, the proposed mechanism is consistent with experimental observations at hand and offers a chemical and physical basis for many of them. Furthermore, if it is correct, it supplies a direct link between the existence of “defective” hemoglobin molecules and the pathological consequences of sickle cell disease."

Linus Pauling. "Sickle Cell Anemia, a Molecular Disease." Science 110: 543-548. April 1949.

"The idea of Dr. Linus Pauling that an abnormal hemoglobin molecule might be responsible for the sickling process initiated the study of the hemoglobin molecule in hereditary anemias."

Harvey Itano. "Clinical States Associated with Alterations of the Hemoglobin Molecule." Archives of Internal Medicine, 96: 287-97, 295. 1955.

"The discovery by Dr. Itano of the abnormal human hemoglobins has thrown much light on the problem of the nature of the hereditary hemolytic anemias, and has changed these diseases from the status of poorly understood and poorly characterized diseases into that of well understood and well characterized diseases"

Linus Pauling. Nomination of Harvey Itano for the Theobald Smith Award. July 1955.

"The demonstration that sickle cell hemoglobin differs in electrophoretic mobility from normal hemoglobin led to the entitled inference: 'Sickle cell anemia, a molecular disease.' This astonishingly simple concept is of fundamental importance to medicine for the ultimate understanding of the origins of sickness, and to biology for the insight into what genes do. In the author's words, 'This investigation...reveals a clear case of a change produced in a protein molecule by an allelic change in a single gene involved in synthesis.'"

Samuel H. Boyer IV. Introduction to "Sickle Cell Anemia, a Molecular Disease." Papers on Human Genetics, 115-25. 1963.

"In 1949, application of methods of physical chemistry directly to the study of a protein produced by a mutated gene led Pauling, Itano, Singer and Wells to identify the specific change in the protein brought about by the gene. The discovery of the first of the abnormal human hemoglobins which they described as causing a 'molecular disease' -- sickle cell anemia -- was followed the identification of a large number of other proteins, each of which owed its difference from normal structure to a mutated gene. Ingram then showed that the change due to the mutation, in the case of each of two abnormal hemoglobins, was confined to a single amino acid residue at one point in one of the polypeptide chains composing the globin. There could be no doubt that genes controlled protein structure by specifying the sequence of amino acid residues in the polypeptide chains. The assumed basic functional correspondence was then altered from 'one gene-one enzyme' to 'one gene-one polypeptide.'"

L. C. Dunn. "Old and New in Genetics." Bulletin of the New York Academy of Medicine, 40(5): 325-333, 329. May 1964.

"I remember asking a new graduate student, Harvey Itano, what his research problem was. He said he was going to test your hunch that there was a difference in hemoglobin molecules between normal people and those with sickle cell anemia. I thought that was a crazy idea; a complicated human disease could not have any such simple cause. And so I learned to respect bold simple ideas -- especially those conceived by Linus Pauling."

Norman Davidson. Letter to Linus Pauling. January 26, 1976.