Trx could bind apoptosis signaling kinase-1 (ASK1) and induce ASK1 ubiquitination/degradation that is not dependent on its redox activity sites (C32 and C35) in ECs, while overexpression of Trx2 increased cell migration and survival by increasing NO bioavailability and inhibiting ASK1-induced apoptosis, and prevented ischemia-induced angiogenesis and hypercholesterolemia-induced ECs dysfunction in mice [65–68]. The gene discussed is MAP3K5; the disease is ischemia.