There also exists a non-genomic pathway; ERs interact with other signaling molecules involved in MAPK or PI3K/Akt pathways.[17,18] Interestingly, at sub-saturating hormone levels, ERβ functions as an inhibitor/competitor of ERα transcriptional activity, suggesting the relative expression level of the ER subtypes determine cellular responses to ER agonists and antagonists.[17,19] Accordingly, the association between ER expression and clinicopathological features of GC differs between ERα and ERβ. The gene discussed is AKT1; the disease is gastric cancer.