It has been well documented that APE is associated with inflammatory response and cell death, which might be mediated by mitogen activated protein kinase (MAPK), Phosphoinositide 3-kinases/protein kinase B (PI3K/Akt), and nuclear factor—kappa beta (NF-κβ) signaling pathways (Apostolakis and Spandidos, 2013; Wang et al., 2013; Wang et al., 2014). This evidence concerns the gene AKT1 and apparent mineralocorticoid excess.