Several studies have explored the PI3K–PTEN–AKT pathway as target for molecular therapy: double mutant BRAF p.V600E and PIK3CA thyroid carcinoma cells lines and xenograft models have heightened sensitivity to combination therapy with simultaneous MAPK and PI3K–PTEN-AKT pharmacological inhibition (144, 145). The gene discussed is AKT1; the disease is thyroid gland carcinoma.