Liu et al. (55) observed p-Akt(Ser473) immunoreactivity in 16/25 follicular thyroid cancers, and found genetic alterations in the PI3K/Akt pathway to account for all of these, including copy gains of PIK3CA, PIK3CB, and AKT2. In anaplastic cancers 16/27 showed p-Akt(Ser473) immunoreactivity. The gene discussed is AKT1; the disease is thyroid gland follicular carcinoma.