Recent advances in molecular biology have allowed population geneticists to make comparisons across species as well as within species. Such molecular information has proven to be an important tool in systematics and in reconstructing phylogenies. Besides just describing past cladogenetic events, it has also been hoped that molecular information could be used to make inferences about the modes of speciation. For example, if genetic revolutions (Mayr, 1954) occur, it has been argued that a large distance based on electrophoretic analyses should rapidly arise between the ancestral and descendant species (Avise and Ayala, 1975, 1976; Avise, 1977, 1978). However, this expectation is made without considering the underlying population mechanisms responsible for speciation and genetic revolutions. Recently, I have investigated both empirically (Templeton, 1979) and theoretically (Templeton, in press) the validity of Mayr's founder effect-genetic revolution model from a population perspective. These studies indicate that a founder effect can indeed induce rapid speciation, complete with preand/or post-mating isolating barriers. However, the details and implications of this rapid speciation are far different from those portrayed by Mayr (1954). Hence, I refer to this mode of speciation as the genetic rather than the genetic revolution to avoid the many connotations the latter phrase has acquired throughout the years. Specifically, Mayr (1954) argued that the founder effect and its associated inbreeding would . . affect all loci at once. Indeed, it was this very genic extensiveness of the founder effect that provides the driving force for the genetic revolution in Mayr's view. Moreover, Mayr (1954, 1955) emphasized that loci were part of a polygenic interaction system in which the marginal effects of a single locus or handful of loci were unimportant. Because of these arguments, the term genetic revolution connotes extensive changes throughout the genome that affect virtually all loci. However, my work indicates this assumption is not true. A transilience does not shake-up the whole genome; rather, it is confined principally to a polygenic system strongly affecting fitness that is characterized by having a handful of major genes with strong epistatic interactions with several minor genes. Indeed, straightforward quantitative considerations imply a transilience would be virtually impossible in a polygenic system lacking a few genes with major marginal effects (Templeton, in press; Lande, in press)just the opposite of what Mayr argues. Hence, all but a small number of genes will be neutral with respect to the transilience, and any expectations concerning distance should be made with this inference in mind. This criticism is particularly relevant since most distance measures are based on enzyme-coding loci, a type of locus that appears to be neutral with respect to the laboratory transiliences I have been studying (Templeton, 1979). (This does not necessarily imply that such loci are neutral in the usual microevolutionary sense.) Moreover, there is much circumstantial evidence that enzyme-coding loci are relatively insensitive markers of speciation and macro-evolutionary events in general (Wilson, 1975; Tauber and Tauber, 1977; Larson and Highton, 1978; Nevo and Cleve, 1978; Ferris et al., 1979; Kirkpat-