Although it remains to be demonstrated how long-term ER stress, perturbation of NF-κB p65 and p53 signaling, and mitochondrial dysfunction in developing endocrine cells may contribute to metabolic diseases like obesity and type 2 diabetes, the platform described here has enormous potential for screening the developmental impact of human exposure to harmful endocrine disrupting chemicals in the environment. This evidence concerns the gene NFKB1 and metabolic disease.