AKT1 and poorly differentiated thyroid gland carcinoma: Alterations in the phosphatidylinositol 3-kinase (PI3K)–AKT (Protein Kinase B) signaling pathway, including changes in Phosphatase and TENsin homolog (PTEN), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), and AKT1, have further clarified the molecular mechanisms driving progression from well-differentiated thyroid carcinomas to poorly differentiated thyroid carcinoma (PDTC) and ATC [20,21,22].