As widely known, the large majority of DTCs are characterized by mutually exclusive driver events, either point mutations or gene rearrangements, involved in the mitogen-activated protein kinase (MAPK) pathway and the phosphatidylinositol-3 kinase (PI3K)/protein kinase B (AKT) pathway.1, 2, 3 In particular, nonoverlapping mutations of BRAF (60%), NRAS (4%), HRAS (1.5%), and KRAS (0.3%) genes are found in conventional papillary thyroid carcinoma (PTC)—that is, those PTCs that grow making papillae—including classical and tall cell subtypes.1, 2, 3. This evidence concerns the gene AKT1 and thyroid gland papillary carcinoma.