In vivo (model of I/R in rats that underwent operation) and in vitro (H9c2 cells exposed to a simulated I/R environment), BBR has reduced myocardial infarct size, improved cardiac function, and inhibited cardiomyocyte apoptosis and oxidative damage, and its mechanism may be related to activation of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway [131]. The gene discussed is JAK2; the disease is myocardial infarction.