There was constitutive activation of mTOR in the patient's original and recurrent tumor, evidenced by phosphorylation (p) of mTOR in a putative site of activation, Ser2448, with a predominantly nuclear distribution most likely indicating an mTORC2 complex (rictor + p-mTOR), [20] and correlative activation of Akt on Ser473 consistent with the presence of both mTORC2 and dominant expression of p-Akt (Ser473) in tumoral nuclei [17], [20], [21]. This evidence concerns the gene AKT1 and neoplasm.