Having demonstrated that hyperglycaemia reciprocally modulated p38 MAPK and Akt activation and thus enhanced myocardial Txnip expression, ultimately aggravating SI/R injury in vitro, we next used a genetic approach to reduce Txnip in vivo to obtain more solid evidence to support a causative role of Txnip and increased myocardial injury. The gene discussed is AKT1; the disease is Hyperglycemia.