Moreover, in cells where IDO2 or IDO1 are overexpressed to levels that deplete tryptophan, inducing autophagy as a result (44), restoring tryptophan is insufficient to relieve protein translation blockades as monitored by a reversal in the expression of the translation stress-induced transcription factor LIP (3, 44), a pathway with pathophysiologic relevance to IDO-driven cancer (45). The gene discussed is IDO2; the disease is cancer.