Additionally, based on our results, the possible molecular mechanism of XBJ in the treatment of CLP-induced SIMI speculated that XBJ’s cardioprotective advantages may be attributable to its ability to suppress apoptosis and promote autophagy via, at least partially, activating PI3K/AKT/mTOR pathway in the early stage of sepsis, as well as promoting apoptosis and inhibit autophagy via suppressing PI3K/AKT/mTOR pathway in the late stage of sepsis. The gene discussed is AKT1; the disease is Sepsis.