EIF2AK4 and neoplasm: Given the importance of maintaining FLIPL levels to prevent apoptosis in cells deprived of glutamine (Fig. 6B, C), all these results suggest that the limitation of glutamine in glutamine-addicted tumor cells will lead, on the one hand, to the elevation of TRAIL-R2 levels mediated by the activation of the GCN2 pathway and, on the other hand, to the decrease of FLIPL as a result of the metabolic defect caused by the loss of αKG.