Mechanistically, this was determined to be due to the downregulation of lncRNA BRAF-activated non-protein coding RNA and the subsequent reduction in thyroid stimulating hormone receptor (TSHR) causing downstream reduction in cyclic adenosine monophosphate (cAMP)/protein kinase A/cAMP-responsive element-binding protein and cyclin D1 that prevents tumor growth downstream of Akt [64,65]. The gene discussed is AKT1; the disease is neoplasm.