The IPA upstream regulator analysis predicted significant activation of the estrogen receptor (ESR1/2), FOS, and STAT3. Prior experience with diethylstilbestrol, a synthetic estrogen, and recent data regarding in utero exposure to estrogenic compounds such as bisphenol A, suggest that developmental exposure to excess estrogen signaling may result in obesity, earlier sexual maturation in girls, and increased risk for breast and other reproductive tract cancers [61], [62]. The gene discussed is ESR1; the disease is obesity due to melanocortin 4 receptor deficiency.