On the one hand, tryptophan depletion caused by high expression of indoleamine-2,3-dioxygenase-1 (IDO1) and tryptophan-2,3-dioxygenase (TDO2) in LN229 glioblastoma cells activated the general control non-derepressible-2 (GCN2) kinase, resulting in phosphorylation of eukaryotic translation initiation factor 2α (eIF2α) and the activation of activating transcription factor 4 (ATF4), which further upregulated WAS expression. The gene discussed is ATF4; the disease is glioblastoma.