Thus, in the presence of stable TCR signaling, costimulatory signaling driven primarily by the PI3K/Akt/mTOR pathway leads to complete T-cell proliferation activation, making inhibition of this pathway and/or TCR signaling a reasonable approach for PTCL therapy [140, 141]. The gene discussed is AKT1; the disease is mature T-cell and NK-cell non-Hodgkin lymphoma.