Activating mutations in the catalytic subunit alpha of phosphatidylinositol-3-kinase (PIK3CA) and in AKT1, and inactivating alterations in the phosphatase and tensin homolog (PTEN), underpin overactivation of the pathway through genetic mechanisms in about half of HR-positive/HER2-negative breast cancers including in Chinese patients15–24. This evidence concerns the gene PTEN and breast carcinoma.