Moreover, since E2 was found to activate the expression of EGR1 in some in vitro cancer studies (Chen et al., 2004; Vivacqua et al., 2012), the increased EGR1 after E2 supplementation could be induced directly by E2 and/or indirectly via reduction of extracellular Aβ(1–42). The gene discussed is EGR1; the disease is cancer.