A specialized piece of in vivo research demonstrated that the antioxidant effect of HSYA was involved in the prevention of Ang II-induced myocardial hypertrophy (a compensatory response to MI), which may act through the activation of the nuclear factor erythroid-2-related factor 2 (Nrf2)/NAD(P)H: quinone oxidoreductase 1/HO-1 signaling pathway (Ni et al., 2018). The gene discussed is NFE2L2; the disease is myocardial infarction.