This tri-pathway cascade, characterized by two-way crosstalk between the oxidative stress response and inflammatory response, points to an integrated signaling axis where enhanced Nrf2 activity attenuates oxidative stress and thereby suppresses NF-κB activation, which in turn prevents NLRP3 inflammasome assembly, underlying the coordinated neuroprotective effects of genistein in models of ischemic stroke [9,10,14,20,23,24,26,29,31]. Here, NFKB1 is linked to ischemic stroke.