  Monod famously once said that what is true of E. coli is true of the elephant, but just as famously, this proved not at all to be the case in moving from prokaryotic to eukaryotic gene regulation. More recently, biologist Bruce Alberts writes: “we can say with confidence that the fastest and most efficient way of acquiring an understanding of ourselves is to devote an enormous effort trying to understand … relatively ‘simple’ organisms” (in Schaffner 1998a, p. 277). What inspires such confidence when a simple organism like C. elegans with its 302 neurons and repertoire of behaviors (movement in response to touch and chemical stimuli, egg laying, and mating) is used to model human behavior in all its complexity? Most importantly, the model organism must be representative of the systems being modeled: genomic sequences must be similar in model and modeled organisms; there must be a known cause-effect relationship between the model organism's genotype and phenotype; there cannot be any “causally relevant disanalogies” between model and modeled organisms, for example, due to differences in complexity (Ankeny 2001, p. S257). Schaffner (1998b) examines molecular geneticists’ use of C. elegans as a behavioral model. Even in these simple organisms, relations between genes, neurons, and behaviors are complex (many-many), with one gene-one behavior associations rare exceptions and their intervening causal chains yet to be understood. While such complexity is to be expected in humans with their more complicated nervous systems, Schaffner believes that there may be a small number of single gene effects on behavior where these genes are highly homologous and strongly conserved—hence, the usefulness of simple models like C. elegans combined with others for investigating basic mechanisms and psychiatric disorders.