Indeed, siRNA-mediated NOP56 KD, which slightly increased ribonucleolar proteins (e.g., NOP58, FBL), markedly induced AKT/mTOR (p-AKT, p-mTOR, pS6), translation initiation (p-eIF4E) and the stress-responsive p38 MAPK in H358 cells in a time-dependent manner (Fig. 3G), as did shRNA-mediated stable NOP56 KD in H358 and H460 cells, but not in KRAS-WT lung cancer H1703 cells (Fig. 3H; Fig. S3G). The gene discussed is AKT1; the disease is lung cancer.