While inhibition of tryptophan conversion to kynurenine using an Ido1 inhibitor also sensitizes fish to infection, similar to Kmo inhibition, the sensitivity can be rescued with exogenous supplementation of kynurenine or 3-HK, suggesting the activity of 3-HK is the primary mechanism of control rather than availability of tryptophan [1]. This evidence concerns the gene KMO and infection.