The phagocytes express β-glucuronidase which accomplishes deglucuronidation (also known as deconjugation) of the flavonoid glucuronide into its aglycone form. The deconjugated flavonoid aglycone subsequently diffuses through the cell membrane where they can reach their target. The mechanism is summarized in Table . For purposes of this review only, the mechanism steps are labeled stages B, C, D, E, and F for clarity. Pathology-selective activation of glucuronide drugs by beta-glucuronidase has been widely understood and exploited in the context of anti-tumor agents. However, it is the "deconjugation in inflammation hypothesis" that was developed and verified progressively over the period 2001-2019 across several polyphenols in vitro, in animal models, and in humans under inflammation conditions. Steps of the pathway were verified across the polyphenols luteolin, quercetin, daidzein, and kaempferol, as well as the ellagic acid metabolites urolithin A, iso-urolithin A, and the single-phenol urolithin B. We propose standardizing the mechanism's naming to the technical term 'deglucuronidation-through-inflammation' or DTI. The 'Shimoi pathway' may also serve as a convenient shorthand that recognizes the lead researcher to first propose and study this mechanism with specific attention to inflammation with polyphenols (by way of luteolin).