The absence of correlation between the two proteins and their divergent behavior led us to hypothesize that, in PTC, the activation of phospho-mTOR might be contributing preferentially to the activation of the mTORC2 complex, and consequently to AKT phosphorylation (phospho-AKT Ser473) [13], as it has been observed in other tumor models [14,15,16,17]. The gene discussed is AKT1; the disease is neoplasm.