IDO1-deficient ApoE−/− mice (ApoE−/−Indo−/−) developed larger atherosclerotic lesions and an unfavorable lesion phenotype.21,35 In addition, inhibition of IDO1 with the IDO1 inhibitor 1-methyl tryptophan (1-MT) led to increased vascular inflammation and aggravated atherosclerosis in ApoE−/− mice.36 Tryptophan 2,3-dioxygenase (TDO) is an isozyme of IDO1. The gene discussed is APOE; the disease is atherosclerosis.