Our objective was to determine the presence and initiation of the KP in DKA’s metabolic and immunologic crisis, and whether it has a potential role in the pathogenesis of the acute vasogenic complication of DKA/BE [6–17] by considering: a) KP’s time proximity to the transient TRP depletion; b) the transition to the formation of kynurenine metabolites and the metabolic/inflammatory cascade relative to the SIR of DKA; and c) whether these KP metabolites might serve as biomarkers of progressing subclinical BE [42, 43]. Here, NPPA is linked to Barrett esophagus.