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Mechanistically, OA suppresses pro-inflammatory cytokines (e.g., IL-17A, TNF-) by inhibiting nuclear factor kappa-B (NF-B) and signal transducer and activator of transcription 3 (STAT3) signaling pathways [8,9,10], attenuates oxidative stress via nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) axis activation [11, 12], and restores immune homeostasis by modulating Th17/Treg balance [9, 13]

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While C677T and A1298C do decrease enzyme activity and make MTHFR function suboptimal, carriers can generally expect to have no trouble converting enough homocysteine to methionine

doi: 10.1126/scitranslmed.3009759