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. The gene discussed is TP53; the disease is obesity due to melanocortin 4 receptor deficiency.