First, Sal B can further induce NLRP3 inactivation by inhibiting intracellular ROS production during myocardial ischemia, increasing the mitochondrial membrane potential, regulating the expression levels of SIRT1, Parkin, and PINK1 proteins, and promoting mitochondrial autophagy (Hu et al., 2020). The gene discussed is NLRP3; the disease is myocardial ischemia.