ER whorls have been shown to form in vertebrate cells exposed to inducers of the ER stress response [10, 13] , and as a result of pathological conditions [14] . Whorl-like smooth ER structures have also been shown to form in mammalian tissue culture cells that over express transfected ER resident proteins or fluorescent protein gene fusions containing heterologous transmembrane domains [15, 16, 17] . Immunofluorescent staining has been used in these transfection experiments to show that weak proteinprotein interactions between the cytoplasmic domains of highly abundant ER imbedded proteins are sufficient to induce membrane stacking and whorl formation. The absence of some ER proteins can also induce whorl formation, suggesting that mechanisms are in place to prevent ER whorls from forming in most cell types [18] .