Breast cancer is often assessed by evaluating activation or inhibition of receptors such as ERα and PR.[37, 38] PR expression is estrogen‐dependent and can modulate the ER activity.[39] Regarding the role of BPA in breast cancer risk, studies have mainly focused on the binding affinity and activity of bisphenol analogs in human nuclear ER,[40] estrogen‐related receptor gamma,[27, 41] GR, AR, and RXR.[42] As early as the 1990s, the determination of PR mRNA and protein expression was primarily used to examine the effects of BPA. This evidence concerns the gene PGR and breast carcinoma.