It has indicated that some mutation events (i.e., BRAF, mitogen-activated protein kinase pathway, etc.)initiate thyroid cancer development and predispose to tumor dedifferentiation while several key nodes (i.e., TERT, TP53, PI3K-AKT-mTOR pathway, etc.)altered promote tumor progression and contribute to tumor aggressivity. Here, AKT1 is linked to thyroid gland carcinoma.