Similarly, when knocking down the endogenous Nrf2 with Nrf2 siRNA, the protective effects of Eze were reversed: the intervention increased infarction volumes and neurobehavioral deficits, reducing the activation of Nrf2 and HO-1, with an associated increase in the levels of TXNIP, NLRP3, Cleaved Caspase-1, and IL-1β. The gene discussed is HMOX1; the disease is infarction.