Increasing the number, regeneration and function of EPCs could promote the repair of damaged endothelial cell monolayers and inhibit mesangial SMC activity and neointima formation, thereby inhibiting atherosclerosis; statins and olmesartan mobilized EPCs in the bone marrow and inhibited endothelial progenitor cell apoptosis through the PI3K/Akt pathways, increasing the number of EPCs in the blood circulation and repairing damaged endothelial cells (Dimmeler et al., 2001; Gong et al., 2015). Here, PIK3CA is linked to atherosclerosis.