The heat-labile enterotoxins of Vibrio cholerae and Escherichia coli induce morphologic changes and steroidogenesis in clonal lines of adrenal tumor cells in tissue culture; these effects are preventable by prior incubation of either toxin with GM1 ganglioside (galactosyl-N-acetylgalactosaminyl [sialosyl] lactosyl ceramide; GGnSLC) but are not preventable by prior incubation of adrenal cells with choleragenoid. Choleragenoid, however, is capable of interfering with the ability of GM1 ganglioside to neutralize the effects of either toxin. These results suggest that the GM1 ganglioside may not be the true receptor for the toxins on adrenal cells, but that it is acting as a pseudoreceptor. The ability of a subunit (A) of the cholera enterotoxin molecule to induce in adrenal cells morphologic changes and steroidogenesis similar to those effects inducible by the whole toxin indicates the possibility that separate receptor sites on these adrenal cells may exist for the binding and active fragments of the molecule.