Analysis of the molecular mechanisms revealed that estrogen reduced the expression of downstream genes, such as AKT, extracellular signal-regulated kinase (ERK) and Janus kinase (JAK) signaling pathways and increased the apoptotic genes (BH3 interacting-domain death agonist (Bid), Caspase-3, Caspase-8 and Caspase-9), through ERβ activation, suggesting that this receptor could have an inhibitory effect in RCC [75,76]. The gene discussed is AKT1; the disease is renal cell adenocarcinoma.