Since the TcR triggering results in rapid activation of PI3K/AKT signaling [39, 40], we decided to investigate if this activation was lower in Mem from the PHI and CHI groups compared to the HIVfree group and if interfering with PTEN, IFN-I signaling or specifically with USP18 would rescue this activation. The gene discussed is AKT1; the disease is congenital isolated hyperinsulinism.