BECN1 and Sepsis: Supposedly, Mel enhances autophagy in sepsis-induced hearts and abrogates cardiac dysfunction and apoptosis [37], and there is also evidence that the overexpression of Beclin-1, an important autophagy initiator, alleviates LPS-induced inflammation and cardiac dysfunction [38]; if so, then Mel-mediated protection in a septic heart results from the activation of autophagy, suggesting that the removal of damaged and dysfunctional mitochondria could be the mechanism by which Mel safeguards against sepsis.