Therefore, selective inhibition of EP4 receptors may avoid the potential gastric adverse effects due to COX-1 inhibition incurred by NSAIDs; (iii) inhibition of EP4 receptors leads to suppression of the PI3K/AKT/mTOR pathway and subsequent tumor cell proliferation; and (iv) inhibition of EP4 receptors leads to polarization of macrophages/dendritic cells from a tumorigenic M2 phenotype to an anti-tumorigenic M1 phenotype. The gene discussed is AKT1; the disease is neoplasm.