Postscript

In this short account of the molecular pathology of hemoglobin we have considered how mutations at or close to the a or P globin genes result in a diverse family of clinical disorders due to the defective synthesis of hemoglobin or its abnormal structure. Work in this field over the last 20 years has given us a fairly good idea of the repertoire of different mutations that underlie single-gene disorders and how these are expressed as discrete clinical phenotypes. Perhaps more importantly, however, the globin field has taught us how the interaction of a limited number of genes can produce a remarkably diverse series of clinical pictures, and something of the basis for how monogenic diseases due to the same mutation may vary widely in their clinical expression.

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