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Instead it works through a distinct set of mechanisms: NFB inhibition: KPV's primary action is blocking NFB, the master switch that drives inflammatory gene expression in immune and epithelial cells

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When SAMe is low, the remethylation of homocysteine to methionine is prioritized in the cell (instead of the transsulfuration pathway).[ref] Drains on methyl groups: About 40% of methyl groups are used for creatine synthesis, so when creatine levels are higher, it can reduce the need for methyl groups