These changes included BZA/CE-mediated downregulation of Plekhs1, a biomarker of glucose intolerance (29) known to be associated with other cancers (30–33); C3, an estrogen-dependent gene involved in the activation of the complement system (34); and Glycam1, a prolactin- and progestin-dependent gene (35). This evidence concerns the gene PRL and Glucose intolerance.