While we did not observe overexpression of estrogen synthetic enzymes or classical estrogen receptor (ER) targets (e.g., PR, AREG, GREB1, or TFF1) (Additional File 1: Table S7) in breast samples from OB ADOL, several additional pieces of data suggested that signaling pathways downstream of the ER may, in fact, be activated in obesity. This evidence concerns the gene GREB1 and obesity due to melanocortin 4 receptor deficiency.