The potential role of inhibited intercellular communication as a mechanism of disruptive differentiation in teratogenesis and carcinogenesis was explored. Gap structure between adjacent cells can be monitored by measurements of electrocoupling, junctional permeability, fluorescent dye transfer, intercellular exchange of metabolites through direct cell contact, and electronmicrograph visualization. The communicating junction appears to be modulated by calcium concentration, acidity, hormones, phosphorylation, and level of cyclic adenosine-monophosphate. Carcinogenic initiators are agents or conditions which can induce stable and irreversible genomic changes, while promoters act as selective mitogens. Chemicals which influence carcinogenesis do not seem to fit into neat categories of pure initiators and promoters. There seems to be a good correlation between depressed junctional communication and cancerous growth. In carcinogenesis, the initiated cell remains inactive until stimulated to proliferate by a tumor promoter. Direct interruption of junctional communication may be a common mechanism of action for tumor promoters that are also teratogens. Parameters that influence teratogenesis are dose, route of delivery, metabolism, embryonic stage of development, and genetic predisposition. Mechanisms involved in teratogenesis include cell death, abnormal membrane characteristics, and altered amounts of metabolic components. Formation and disappearance of gap junctions have been associated with major morphogenic events in several embryonic species and tissues. Inhibition of gap junction mediated communication may interfere with embryonic development. Direct intercellular communication is a likely method to control distribution of small morphogenic substances. Inhibitory signal may be transmitted through the gap junction. Several teratogens interfere with gap junction mediated metabolic cooperation.