Nearly two decades ago, Richard Dawkins proposed the concept that genes possess an inherent property of “selfish replication.”1 He argued, anthropomorphically, that these basic units of heredity behave in a manner that guarantees their self-perpetuation. However, a flawed gene would be eliminated from the species by selective pressure against the expression of a deleterious trait. Thus, only the most robust genes would be transmitted to subsequent generations. In this issue of the Journal, Greengard and her colleagues2 describe a homozygous mutation in the gene for coagulation factor V that seems to have no adverse clinical effects. Their report suggests that . . .
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Katherine A. Hajjar (1994) studied this question.
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