IHC of the PF139 residual tumors revealed that NOP56 depletion plus rapamycin strikingly suppressed tumor cell proliferation (Ki-67) and dampened mTOR activity (p-AKT, p-mTOR and p-S6), but increased Caspase-3 cleavage (Fig. 6I), which is consistent with the in vitro results (Figs. 4, 5) and our observations on H460 xenografts (Fig. S5A). The gene discussed is AKT1; the disease is neoplasm.