Vitexin inhibits vascular inflammation by directly binding to the Kelch domain of Keap1, breaking the Keap1-Nrf2 connection, and releasing Nrf2 for transport to the nucleus, highlights a new function for Nrf2 in vascular inflammation and offers intriguing molecular pathways for innovative approaches to treating metabolic and cardiovascular disorders [28,63]. Here, KEAP1 is linked to cardiovascular disorder.