By analyzing the effects of zinc on growth and dimorphism, it has become clear that there exists at least two modes, or "pathways," of mycelium formation in C. albicans (7). Paradoxically, even though the characteristics for the two modes appear to be opposite in nature, the mycelium that form appear to be superficially similar. Unfortunately, it may be difficult to compare the two modes unambiguously at the molecular level for two reasons. First, the physiology of cells resuming growth after release from stationary phase will undoubtedly differ drastically from the physiology of cells exiting from the growth cycle, regardless of phenotype. Therefore, most molecular or physiologic differences probably will represent differences in growth rate or position in the cell cycle, rather than alternate molecular mechanisms that are basic to the alternate modes of mycelium formation. Second, it has been observed that during release from stationary phase, a prescribed program of gene expression accompanies commitment to the mycelial and budding forms (11). This program was demonstrable because of the excellent synchrony and homogeneity of released cultures (60), which is a characteristic lacking in cultures entering stationary phase in the M10 mode. Even so, a comparison at the molecular level between the two modes of mycelium formation should be undertaken with the above reservations in mind. Perhaps the most attractive aspect of alternate modes of mycelium formation in Candida is at the genetic level of analysis. The hypothesis of homozygosis in the expression of the M10 phenotype is testable, as is the possible role of the M10 phenotype in tissue penetration. If the hypothesis is true and if the M10 phenotype predominates in infected tissue, it would represent a new mechanism of opportunism in infectious fungi that may be used by other systems as well as Candida. If it is not true, a detailed analysis of the differences between the two modes of mycelium formation will still be valuable in our understanding of both the mechanisms regulating phenotypic transitions in Candida and the more general question of cell divergence in developing systems.